NUGGETS

INTERNAL MEDICINE FOR USMLE STEP-2

By: Shaheryar Ali Jafri

DEDICATED TO

HEMATOLOGY, ONCOLOGY & SOME GENETIC

DISEASES
1) A person with combination of Microcytic Anemia + Renal failure + Neurological
deficit = LEAD POISONING Causes: can be ingested, inhaled or absorbed through
skin.. a) Occupational exposure(solder, paint, car-radiator, battries, smelting, lead
glazes, refining) ; b) In children: Eating lead paint, old housing, urben dwellers
Other clinical features: Abdominal pain, constipation, dementia, fatigue, Myalgia,
Lead nephropathy, Peripheral neuropathy (extensor weakness=wrist drop, foot drop),
Hypertension, Poor cognition..
Diagnosis: Blood lead levels =>10ug/dl=poisoning.. Peripheral blood smear:
Basophilic stripping (Note: basophilic strippling also found in Megaloblastic)
Treatment: EDTA, Succimar (oral), Dimercaprol (BAL), penicillamine
LEAD POISONING IN CHILDREN
(People shift to new place which is being renouvated and painted)v.imp mcq
Behavioural changes (most common)
Young: Hyperactivity
Older: Agression
Cognitive/ Developmental
GIT
Anorexia, pain, vomiting
CNS
High risk for lead poisoing: children, houses built before 1978, international adoptees and
immigrants. Best Screening test: finger stick. Normal levels <5ug/dL. Preventive measure
are taken in those who have levels 5-44. Treatment is given in those who have lead levels
>44. 45-69 give PO succimer(DMSA). =/>70 ug/dL is medical emergency (cerebral
edema); give IM dimercaprol (BAL) and then followed by Iv EDTA.
Before giving DMSA: order LFT, FEP to monitor response and follow up in one month with
repeation of these test along with blood lead levels
Also add iron and calcium supplements as they inhibit the absorption of lead
2)
A
patient
with
ANEMIA+JAUNDICE+SPLENOMEGALY+CALCULOUS
CHOLECYSTITIS+FAMILY HISTORY = HEREDRITY SPHEROCYTOSIS Autosomal
dominant b/c of FRAME SHIFT MUTATION in RBC membrane cytoskeleton ANKYRIN &
SPECTRIN.. RBC become fragile and EXTRAVASCULAR HEMOLYSIS is also its feature
leading to INCREASED RETICULOCYTE COUNT MCHC and RDW is also
increased..MOST ACCURATE TEST: OSMOTIC FRAGILITY TEST Rx: Folate
supplementation (V.IMP MCQ) and Splenectomy.. (After splenectomy = smear will show
HOWEL JOLLEY BODIES)

CHOLECYSTITIS+SPLENOMEGALY+FAMILY HISTORY = HEREDRITY SPHEROCYTOSIS

The most feared long term complication of SPLENECTOMY= SEPSIS with

encapsulated bacteria (s.pneumoniae, h.influenzae, Neisseria) most common
sepsis by STREP PNEUMONIAE.. B/c of impaired antibody mediated
OPSONIZATION & PHAGOCYTOSIS) MTB2: 214
2 weeks before splenectomy = give Pneumovax for strep.pneumoniae,;
meningococcal vaccine; and also Hib if patient not got in childhood......... if
splenectomy has been performed in emergency i.e for trauma = give these
vaccines as soon after surgery before discharge.
After surgery a DAILY ORAL PENICILLIN is recommended for 3-5 years. b/c the
risk of pneumococcal sepsis persists for >10 years (even almost 30 years or may
be lifelong)..v.v.v.v.v.imp MCQ (kyunki strep pneumonia ka sepsis kafi shaded
hota ha)
Never perform cholecystectomy in suspected/confirmed hereditary spherocytosis
before removing the spleen ( risk of inta-hepatic stone formation)

3) Hepatosplenomegaly+ Anemia +Thrombocytopenia = GAUCHER DISEASE =

Autosomal recessive; Caused by deficiency of B-glucocerebrosidase .. hence lipid laden
macrophages accumulate in liver, spleen, bonemarrow.. Other Clinical features = Bone
pain, Aseptic necrosis of femur, Erlenmeger Flask deformity.. Dx: Microscopy shows
Gaucher cells (Macrophages with eccentric neucleoli with PAS + inclusion bodies
resembling CRUMPLED TISSUE PAPER.. Rx: Enzyme replacement therapy = alphaglucerase

Erlenmeyer Flask deformity of distal femur

4) Mental retardation + Developmental delay + Neurodegeneration+ Cherry red spot on
macula = D/D = i) Niemann pick disease ii) Tay-Sachs disease. (AR)
Nimen pick
Hepatosplenomegaly

Tay sach
No hepatospleno

Deficency of Sphiingomyelinase
Foam cells having Zebra bodies

Deficency of Hexosaminidase A
Onion skin lysosomes
Hyperacusis
Naeema moti ha so usko hepatosplenomgealy ha isi lea wo Zebra pe safar krti ha= NIMEN
PICK HAS HEPATOSPLENOMEGALY while TAY-SACH no

5) A patient with megaloblastic anemia = must differentiate b/w folate deficiency and
B12 deficency. B12 deficency can occur after total or partial gastrectomy b/c of
deficiency of intrinsic factor and also from Autoimmune gastritis A (pernicious anemia);
Strict vegetarian also develop B12 deficency (v.imp) .. B12 is necessary for DNA
synthesis I.E converts methyl-tetrahydrofolate into Tetrahydrofolate (not hemoglobin
synthesis) v.imp mcq
The most common neurological finding in B12 deficency is peripheral neuropathy and the
least common is Dementia.. B12 def also presents with GLOSSITIS and DIARRHEA.
(v.imp mcq)
After B-12 replacement therapy RETICULOCYTE
NEUROLOGICAL ABNORMALITIES improve last.

count

improves

first

while

B12 (pernicious
Folate
B12 levels
Decreased
Normal
Folic acid levels
Normal
Decreased
LDH levels and bilirubin
Increased
Normal
Acholhydria
Present
Absent
Schilling test
Positive
Negative
Methylmalonic acid in urine
Present
Absent
Neurological signs
Present
Absent
Homocystine levels
Increased
Increased
Cause of deficiency
i) Gastrectomy
i) Tea and toast diet
ii)
Autoimmune ii) Alcholosim
gastritis
iii) Drugs: methotrexate
iii) Strict vegetarian
Megaloblastic anemia can give anisocytosis, poikilocytosis and basophilic stippling.
RETICUOCYTE COUNT is decreased although bone marrow is hypercellular.
Hypotyroidism, Liver disease, Fanconi anemias and some anti-metabolites(5FU, AZT,
hydroxyurea) also give non-megaloblastic macrocytic picture.
Increased MCV = Macrocytic anemia
Increased MCV with hypersegmented neutrophils = Megaloblastic anemia
Dx: i) Best initial test = CBC with peripheral blood smear

ii) Most accurate test = B12 levels and RBC folate levels. But B12 is acute phase
reactant and also can increase in inflammation. So if such condition is there. Do
methylmalonic acid levels What is the next best test to confirm the etiology of B12
deficency if its levels found low??
............. ANTI-PARITETAL CELLS and ANTI-INTRINSIC FACTOR antibodies
6) An old patient with Ecchymotic lesions on areas susceptibe to trauma (dorsum of hand
and forearm) = SENILE PURPURA Cause: Perivesicular connective tissue atrophy.
Lesions develop rapidly and resolve over several days and leave a hemosiderin laid
brownish discoloration
7) A woman with history of recurrent 1st trimester miscarriage + Positive VDRL +
Prolonged APTT + Thrombocytopenia = ANTIPHOSPHOLIPID ANTIBODY SYNDROME..
Treat pregnant woman with LMWH..
8) Bone tumorsEpiphysis, Metaphysis, Diaphysis (GOE)
i) Giant cell tumor = Epiphysisesp around knee joint. X-ray = Soap bubble appearance
due to osteolysis.More common in female 20-50 yearsIt is benign tumor but is highly
aggressive and recurs after surgery so High expert orthopedic surgeon should deal with
it.
ii) Osteosarcoma = Metaphysis = X-ray shows codman triangle/sun burst appearance/
osteolytic lesion/ periosteal inflammation or elevation. Labs show only elevated
ALP but ESR is normal b/c this tumor is not associated with systemic signs.
iii) Ewing sarcoma = Diaphysis = X-ray shows osteolytic lesion with onion peel
appearancepatient as more systemic signs (fever, malaise, weight loss).Mutation of
t(11;22) EWS-FLI1. Origin from neuroectodermal cells giving uniform round blue cells
in rossettee pattern.
9) POLYCYTHEMIAS
Polycythemia vera
(

i) Malignant clonal proliferation of hematopoietc stem cells

ii) Increase in RBC mass, independent of erythropoietin
iii) Pruritis after taking bath, facial plethora
iv) Symptoms of Hyperviscosity: headache, dizziness,
impairment, dyspnea
v) Thrombosis: DVT, CVA, MI, portal vein thrombosis
vi) Hepatosplenomgealy
vii) Hypertension (v.imp MCQ), Gout, peptic ulcer

visual

viii) Dx: A) CBC: inc RBC, HEMATOCRIT, HEMOGLOBIN, thrombocytosis,

leukocytosis.. b) Decreased erythropoietin
c) Elevated VITAMIN B12 and URIC ACID
Rx: Repeated phelobotomy
Supurious polycythemia Plasma volume contraction (diarrhea, vomiting, decreased oral intake)
Polycythemia due to CO
poisoning
Polycythemia due to Eg in OBSTRUCTIVE SLEEP APNEA , OSLER WEBER RENDU
hypoxia
(Reactive SYNDROME(RL
shunt
causing
pulmonary
hypertension___>
polycythemia)
hypoxemia. Polycythemia)

10) A patient on a routine X-RAY found to have a coin lesion on LUNGS. How will you
proceed? ASK FOR PREVIOUS X-RAY and classify patient into low risk and high risk..
Low risk: Age <35 years, Non smoker, <2cm lesion, smooth margin, no change in last
12 months evident by previous x-ray.. Now follow them with CXR every 3 months
for 12 months.
High risk: opposite to above.. Follow by CT scan.. FNAC if missed on fnac do
open lung biopsy
11) Central Lung cancers = Squamous cell, Small cell
12) Peripheral Lung cancers = Adenocarcinoma, Large cell Bronchoalveolar
carcinoma can give multiple nodules Adenocarcinoma is associated with pleural effusion
having HIGH HYALURONIDASE LEVELS.
13) The most common symptom of lung cancer = Cough. . Other: Weight loss,
dyspnea, hemoptysis, recurrent pneumonia, chest wall pain, Pancoast tumor, Horner
syndrome,
Pleural
effusion,
SVC
syndrome,
Paraneoplastic
syndromes
(Hyperparathyroidism, SIADH, Eaton lambort, Hypertrophic osteoarthropathy)
Note:i) Treat SVC syndrome with Radiotherapy
ii) Hoarsness, Effusion, Extrathoracic spread make the tumor UNRESECTABLE but
only exception is a single metastatic deposit to brain which can be removed surgically
followed by whole brain radiation (v.v.v.imp)
iii) Tumor can also invade in to brachial plexus like pancoast tumor and it can lead
to pain in arm (
iv) A chronic smoker with horner syndrome = LUNG CANCER.
14) A child with Aplastic anemia; increased MCV, absent radius, hypoplastic thumbs,
hyper/hypopigmentation of skin, Caf-ai leut spots, microcephaly, pounding in the ears,

short stature = FANCONI ANEMIA.. It is autosomal recessive caused by

CHROMOSOMAL BREAKS (v.imp MCQ)
15) A child with Pure RBC aplasia, Increased MCV, ----, Triphalangeal thumbs, Short
stature = DIAMOND BLACKFAN SYNDROME.. It is characterized by absence of erythroid
precursor cells in bone marrow and also no reticulocytes but increased ADA levels..
Pure RBC aplasia can also be associated with THYMOMA (v.v.v.imp), SLE, leukemia,
parvovirus B 19)
16) Hemolytic anemias may be due to Intrinsic RBC defect or Extrinsic to RBC causing
hemolysis
Intrinsic
i) Membrane (Heredrity spherocytosis, PNH)
ii) Enzyme (G6PD, PK def)
iii) Hemoglobin (Thalassemia, Sickle cell)
Extrinsic
i) Immune: Cold AIHA, Warm AIHA
ii) Non-immune: Traumatic (Prosthetic heart valves), MAHA (TTP, HUS,
DIC)
Lab findings in
CBC
Peripheral
blood smear

RBC indices
Other

hemolytic anemias:
Hb, Hct, RBC, Reticulocyte count
Large reticulocytes,
i) Heredrity spherocytosis: Hyperchromic spherocytes
ii) PNH:
iii) G6PD def: Heinz bodies and Bite cells
iv) Traumatic and MAHA: Schistiocytes, Halmet cells
MCV = normal but sometimes b/c of large reticulocytes
LDH, Bilirubin,
Intravascular: Haptoglobulin, Haemosidrinuria, Hemoglobinuria

Sickle Cell Anemia

sepsis
by
encapsulated
bacteria
(strep.pneumoniae)

i) Autosomal recessive; glutamic acid replaced by valine (HbS)

ii) Patients are protected against falciparum malaria
iii) As deoxygenated HbS polymerizes and forms crystals and
sickling of RBC and membrane damage leading to extravascular
hemolysis also sticky nature causes occlusion of blood vessels
iv) Clinical features: Hemolysis, Jaundice, Gallstones, Leg ulcers,
splenomegaly then autosplenectomy, Osteomyelitis (Salmonella),
Renal failure, Papillary necrosis, TIA, Retinopathy, MI,
Cardiomyopathy, Acute chest syndrome (Chest pain, hypoxia,
lung infiltrates), Aplastic crisis (Parvovirus B19, folate def:
worsening anemia with Retic b/c of transient arrest of

HbC
disease:
GLUTAMIC
ACID
REPLACED
BY erythropoiesis; platelet and wbc may be normal but retic count is
LYSINE
absent), Acute painful crisis (Dactylitis, pain in rib, back,

Scenario may be:

An
African
American
patient
with sudden onset
of severe pain in
chest, back, thighs,
may
be
accompanied
by
fever.

elbows, knees/ x-ray: soft tissue swelling/ osteolysis. Cause

is Vaso-occlusion of vessels ..)

50 % develop OSTEONECROSIS = pain in hip which is

progressive but there is no tenderness and limitation to internal
rotation(pain and functional limitation) commonly affecting
humerus head and femoral head

Inv: i) PBC: howel jolly bodies, sickle cells, Reticulocytosis ,

macrocytosis (b/c of increased demand of folic acid) ii) XRAY: fish mouth vertebrae Best initial test: Peripheral blood
smear / Sickledex Most accurate test: Hb Electrophoresis
showing HbS >80%
In aplastic crisis Retic count decreases suddenly so to
check for parvovirus B19 infection = best initial test is
Reticulocyte count (MTB-2 page: 215)
Rx: Same as for splenectomy (vaccination), folate
supplementation,
i) For acute painful crisis: Hydration, analgesia, Oxygen, If temp
increase (Antibiotics: 3rd ceph, flouro)
ii) For acute chest syndrome, stroke, splenic crisis, before
surgery: above + RBC exchange transfusion
iii) If recurrent >3 episodes of crisis, symptomatic anemia, life
threatning complication: HYDROXYUREA to prevent recurrences
of acute painful crisis and acute chest syndrome (as it increases
HbF levels which sickling)
iv) If recurrent acute chest syndrome/stroke = Bone marrow
transplant
v) For acute stroke = EXCHANGE TRANSFUSION

. One of the known side effects of this medication is

myelosuppression, which should be monitored regularly with a
complete blood count. It is also important to monitor liverfunction tests for hepatotoxicity. Fetal hemoglobin concentrations
are measured to evaluate response to the therapy not to evaluate
for toxicity.
Sickle Cell Trait
Asymptomatic to hyposthenuria with nocturia/enuresis,
hematuria from renal papillary necrosis (v.imp mcq) ,
asymptomatic bacteriuria/ risk of pyelonephritis (especially
8%
African during pregnancy), possible PE and/or glaucoma acute vasoAmerican are sickle occlusive crises in periods of extreme hypoxia and/or acidosis or
cell trait positive
dehydration; Lab findings normal; Blood smear normal; most

accurate diagnostic test =Hb electrophoresis with HbS > 35%

but < 50%; treatment not required

G6PD deficiency

Note: Hyposthenuria is due to RBC sickling in the vasa rectae of

inner medulla which impairs counter-current exchange and free
water absorption. These PATIENTS ARE THEREFORE ADVISED
TO AVOID DEHYDRATION B/C PATIENT WILL PRODUCE DILUTE
URINE EVEN DURING DEHYDRATION LEADING TO SEVER
WATER DEPLETION (MTB-2 PAGE: 307)
In all patients of SICKLE CELL ANEMIA= give Pneumococcal
vaccine and Penicillin prophylaxis for 5 years
i) X-linked recessive
ii) Ppt by Infections, drugs (sulfonamides, nitrofurantion,
primaquine, dimercarol, fava beans)
iii) c/f: episodic hemolytic anemia, dark urine, jaundice,
iv) PBS: Bite cells, Heinz bodies
v) G6PD levels may be normal during the episode of hemolysis.

TTP
Etiology

Idiopathic ass with HIV,

ticlopidine,
cyclosporine,
pregnancy
ADAMTS13 activity
(protease that cleaves large
vWF multimers secondary
to
IgG
autoantibody
production
c/f
Pentad
i) MAHA
ii) Acute renal failure
iii) Thrombocytopenia
iv) Fever
v) Neurologic (headache,
seizure)
Treatment
Plasma
exchange
(Plasmapheresis, FFP)
V.V.V.IMP MCQ + steroids
+ Dypyridamole
Never ever give antibiotics and Platelet transfusion

HUS
E.coli O157:H7 (Hamburgur)

Triad
i) MAHA
ii) Acute renal failure
iii) Thrombocytopenia

Supportive,
Steroids,
antiplatelets if severe = plasma
exchange

17) A post-op-patient on NPO and after 7 days bleeding from venipuncture site with
Increased PT and APTT (PT>>>APTT) = Vitamin K deficiency.. Normal body has 30 day
store of Vitamin K but if severly ill ; within 7 days stores get depleted.
Causes of Vit.K deficiency: Malabsorption, NPO, prolonged antibiotic use, dietary
deficiency, Warfarin therapy, Hepatocellular disease.
,
18) Hypercalcemia: CHIMPANZEES (Calcium ingestion, Hyperthyroid-parathyroid,
Iatrogenic (thiazide), Multiple myeloma, Pagets disease, Addison disease, Neoplasm,
Zollinger elisson(MEN-1), Excess vit D, excess vitamin A, Sarcoidosis.,. Patients with
Pagets disease are usually normocalcemic but become hypercalcemic if they are
immobilized.
C/F: Stones, bones, groans and psychiatric moans if hyperparathyroidism (Osteitis
fibrosa cystica), constipation, polyuria, muscle weakness, Cl/P ratio >33:1, ECG:
shortened QT interval.
Rx:
i) For hypercalcemic crisis: vigorous IV fluids then furosemide..If still elevated = Give
Calcitonin What is mechanism of calcitonin? Decrease absorption of Calcium from
kidney and GIT, Decrease bone resorption by inhibiting osteoclasts
ii) If sarcoidosis: Steroids
iii) If due to malignancy (M.M, breast) = Bisphosphonates (Zolendronic acid) v.v.imp
mcq (all women with metastatic breast cancer should receive I/v
BISPHOSPHONATE).. These are osteoclast inhibitors
19) An old patient with back pain, repeated infections, Bone fractures, anemia,
hypercalcemia, renal failure (due to obstruction of DCT & collecting ducts by Paraproteins
(Bence jones proteins), lytic lesions on X-RAY, no sings of hyperviscosity and protein
electrophoresis (best initial test) show Monoclonal IgG M-spike >4g/dl =
MULTIPLE MYELOMA.Gold standard test: Bone marrow biopsy >10% plasma cells..
Best initial treatment: Talidomide and Steroids Most curative therapy: Autologous
stem cell transplant .
But before transplant: give Vincristine, Adriamycin, Dexamethasone For relapsing
disease = Bortezomab. To check response to therapy: B2 microglobulin If
signs of cord compression: Radiotherapy
Note: There is a PARAPROTEIN GAP in patients with multiple myeloma (TOTAL PROTEIN
ALBUMIN = >4g/dl) b/c defective proteins are made inspite of albumin.

20) Asymptomatic patient with monoclonal IgM M-spike<3g/dl , bone marrow shows
<10% Plasma cells = MGUS (but 1st exclude all findings of multiple myeloma doing
SKELETAL SURVEY (X-RAY) no lytic lesions
21)Old patient with signs of Hyperviscocity eg: on ophthalmoscopy=engorgement of
retinal veins, bleeding from mucosa and GIT, brusises on body, Hepatosplenomgealy,
Headache, night sweats, Tierdness, Anemia, Pain and numbness in exteremities (b/c of
demyelinating neuropathy) and no other signs of multiple myeloma, protein
electrophoresis showing Monoclonal IgM M-spike >5g/dl = WALDENSTROMS
MACROGLOBULINEMIA (Plasma cells invade marrow and can cause aplastic)
Best initial treatment = Plasmapheresis
Further: as CLL (Fludarabine, Chlorambucil)

22) Pain, tenderness, induration, erythema along the course of a vein with PALPABLE
TENDER CORD = Superficial thrombophelibitis(STEP-UP PAGE: 62). Causes: IV
infusion, varicose veins. When superficial thrombophelibitis occurs in different
locations over a short period of time esp on atypical sites eg: Arm, Chest= Think of
MIGRATORY SUPERFICIAL THROMBOPHELIBITIS (TROSSAEU SYNDROME) most
commonly associated with PANCREATIC CARCINOMA.. (as it releases procoagulants
and platelet aggregating factors) if u suspect trossaeu syndrome = DO
ABDOMINAL CT to diagnose underlying occult malignancy. V.v.v.imp mcq
23) An old patient with Leukocytosis+anemia+ Increased number of Mature granulocytes
in blood, marked Basophilia, splenomegaly = CML.(it is the only leukemia giving
increased PLATELETS), Phildelphia chromosome.. t (9;22), 3 phases i) Chronic
phase, ii) Accelerated phase iii) Blast crisis.Lab: LOW LEVELS OF LAP (Leukocyte
Alkaline Phosphatase) (LAP also low in Hypophosphatemia, PNH) Rx: Tyrosine
kinase inhibitors (Imitanib, Dasatinib, Nilotinib)
24) Fair skin person with sunlight exposure, S-100 positive = MALIGNANT MELANOMA.
Dysplastic naevus is a precursor Depth of tumor correlates with the risk of
metastasis and it has dark irregular border. (BRAF KINASE MUTATION braf kinase
inhibitor=VEMURAFENIB)
Risk factors: fair skin, male gender, xeroderma pigmentosum, sunburn, Large number of
moles, Dysplastic nevus syndrome, Giant congenital nevi.
C/f: ABCDE (Assymetry, Border irregular, Color variegation, Diameter >6, Elevation)
Most common site: BACKDx: Excision biopsy.
Metastasis: Lymph nodes, skin, Lung, Liver, Brain (common cause of death), Bone, GIT

Note: i) Brain metastasis from Malignant melanoma gives BLEEDING INTRACRANIAL

LESION.(V.V.V.IMP MCQ)
ii) Tumors that metastasize to brain: Lung, Breast, Melanoma, Kidney, GIT. Important
to note that PROSTATE do not metastasize to brain although it goes to cranial cavity.
iii) Malignant melanoma is called The fascinating disease. It cangot tho the most
unimaginable sites and can remain dormant for 15-25 years and recur in surprising ways.
25)
Bone
Breast
Tamoxifen Agonist
Antagonist
Raloxifene Agonist
Antagonist
Note: Tamoxifen has an increasd risk of
sarcoma. (

Uterus
Use
agonist
ER +ve breast cancer
Antagonist Post-menupausal osteoporosis
causing endometrial carcinoma and uterine

26) Microcytic hypochromic anemia with increased RDW(>20) and Low Reticulocyte =
IRON DEFICENCY ANEMIA (
27) Microcytic hypochromic anemia with norlam RDW but Increased Reticulocyte =
Thallasemia
28) >50 year old patient with microcytic hypochromic anemia = may be colon cancer =
DO COLONOSCOPY. Normally screening with colonoscopy is recommended for every
person who reaches 50 years and repeat every 10 years.
i) If a close family member has had the disease = start screening at 40 or 10 years earlier
than the family member was diagnosed, whichever is earlier
ii) HNPCC is defined as colon cancer in 3 family members in 2 generations having the
disease, with 1 having it <50 years in this case, start screening at 25 years of age
and repeat every 1-2 years.
29) A patient esp Female with mucosal and deep bleeding, heavy menstrual bleeding,
Labs showing PROLONGED BT and aPTT but normal PT = von-WILLEBRAND DISEASE.
Autosomal dominant.Ristocetin assay is abnormal in it.
Rx:
i) Mild bleeding: Desmopressin (DDAVP) v.v.vimp mcq (it releases v.wb factor from
endothelium)
ii) Mucosal bleed: Tranexamic acid
iii) Cryoprecipitate
iv) Do not use aspirin

v) In women: OCP estrogen

30) A child with pallor, hepatosplenomegaly, anemia, chipmunk facies, frontal bossing =
BETA THALLASEMIA MAJOR
Major
Intermedia
Minor
Homozygous
/ +
/
/
+/ +
/ +
After 6-9 months, anemia is Less symptoms
Asymptomatic
manifested
Always
need
blood Sometimes need blood No
transfusion
transfusion
hemoglobin F is increased
HbA2 is increased
Note: i) there is a subtype of sickle cell disease HbS-Beta thalassemia disease
characterized by percent hemoglobin F > hemoglobin S>hemoglobin A.
ii) Patients with sickle cell disease should promptly initiate penicillin prophylaxis.
Recurrent sickling in the spleen leads to decreased immunity to encapsulated organisms
such as streptococcus pneumonia and Neisseria meningitides and eventually to autoinfarction of the organ. Children should receive all of their routine childhood vaccinations
on a normal schedule. In addition, they receive annual meningococcal vaccine once they
are > 6 months of age and a pneumococcal polysaccaride vaccine at two years of age.

GENETIC DISORDERS

1) Newborn with meconium ileus/ Child with failure to thrive, recurrent pulmonary
infections (bronchiectasis, pseudomonas, staph), rectal prolapse / man with infertility/
chronic bronchitis/ Pancreatic insufficiency (malabsorption and stateorrhea)..
CYSTIC FIBROSIS.Dx: Increased concentration of Chloride ions in Sweat. (NBME:
2:22), Best initial test and most accurate (2 elevated sweat chloride conc >60mEq/L
obtained on separate days. If SwEAT TEST IS EQUIVOCAL WHAT TEST

WILL YOU DO? DO POTENTIAL DIFFERENCE B/W NASAL EPITHELIUM WHICH

WILL SHOW INCREASED POTENTIAL DIFFERENCE; Or may can do genetic
studies
(KAPLAN: 83)
Newborn screening method= TRYPSINOGEN
.. MTB2 : 140.. MTB3 P=350
Cause: AR, dfct in CFTR gene on chromosome 7 b/c of DELETION of three base pair
encoding for phenylalanine (DF508)
Sputum me mostly staph milta ha but infection mostly pseudomonas krata ha
AS IT IS A.R DISEASE. IF ONE AFFECTED CHILD; CHANCE OF ANOTHER
AFFECTED CHILD
Note: Normally CFTR secretes Cl ions in GIT and Lungs while absorb Cl from sweat.
Respiratory
i) Nasal polyps
ii) Pulmonary mucoviscidosis (thick mucous)
iii) Recurrent infections with Staph and Pseudomonas, Allergic
bronchopulmonary aspergillosis
iv) Examination: AP diameter, Hyperresonance, rales, clubbing,
wheeze, cyanosis, sinusitis
v) X-RAY: Hyperinflated lungs(imp mcq), Nodular densities, patchy
atelectasis, confluent infiltrates, progression (flattening of diaphragm,
sternal bowing, narrow cardiac shadow, cysts, extensive
bronchiectasis (Tram tracking)
vi) PFTs: <5 years = obstructive >5 years: restrictive
Genitourinary i) Delayed sexual development
ii) Azospermia (95%), 20% absence of Vas Defernc
iii) Hernia, hydrocele, cryptorchidism
iv) Secondary amenorrhea and cervicitis in females
v) women are infertile b/c of thick cervical mucus
Sweat glands Chloride in sweat and increased risk of dehydration

Abdominal

Signs
vitamin
deficencs
adek
Rx

Newborn: meconium ileus(most common initial presentation)

Older: Rectal prolapse, pancreatic insufficiency, Biliary cirrhosis,
Diabetes, pancreatitis, prolonged jaundice at birth
of Epistaxis ( vit k)

i) Nutrition, pancreatic enzyme supplements, vitamins, chest physio

ii) For acute exacerbation of resp inf (
: Pipercillin + Gentamicin / Pipercillin + Tobramycin or Ceftazidime (to
cover pseudomonas)
iii) Human recombinant DNAse daily (mucolytic)
Inhaled aminoglycosides only used in CF

Routine
antibiotics
Inhaled
Rh DNAse (breaks massive amount of DNA in respiratory mucus)
Bronchodilator Inhaled albuterol
Vaccines
Pneumococcal and Influenza

2) Patient with recurrent epistaxis, skin discoloration, ruby colored rED papules in lips and
trunk, telangectasias, AV malformations (mucous membrane, skin, GIT, liver, lung,
brain).. HEREDRITY HEMORRHAGIC TELENGECTASIA (OSLER WEBER
RENDU SYNDROME).. AUTOSOMAL DOMINANT
Lung: AV malformation cause RIGHT TO LEFT SHUNT..leading to chronic hypoxia.
Reactive polycythemia these AV malformation can also cause hemoptysis
3) Child with mental retardation, Attention problem with hyperactivity, Xtra large Testis,
Jaw, Ears, Autism, Mitral valve prolapse/ aortic root dilatation (vimp association)
= FRAGILE X SYNDROMe. X-linked recessive (Breakage on Long arm of chromosome
x) affecting methylation and expression of FMR1 gene due to trinucleotide tendem repeat
CGG. Other features: short attention span, joint laxity..Confirmatory test: DNA
molecular analysis for trinucleotide repeat
Goljan: 88, 1st aid: 87

4) Child with mental retardation, Hyperactivity, Small jaw, maxillary hypoplasia, short
nose, Smooth Long philtrum, microcephaly, thin and smooth upper lip, Behavioural
abnormalities, Joint abnormalities, Cardiac (VSD>ASD), growth retardation, Mother
history of Alcoholism = FETAL ALCOHOL SYNDROME
5) A child with triad of TIE. Thrombocytopenic purpura, Infections recurrent, Eczema
= WISKOTT-ALDRICH SYNDROME X-LINKED RECESSIVE leading to progressive
deletion of B and T cellsmost common manifestation is low platelet count b/c of
decreased production(<50 thousand).Labs: platelets, IgM, IgA, E
Note: Initial manifestations often present at birth consists of petechiae, bruises, bleeding
from circumcision, bloody stools

SEXUALLY TRANSMITTED DISEASES

1) Painful genital Papule or Pustule along with painful inguinal lymphadenopathy. Ulcer
giving appearance of irregular, deep, well demarcated, necrotic satellite shaped, 1-3 in
number. CHANCROID caused by Hemophilus. Ducreyi Treat with
AZITHROMYCIN or CEFTRIAXONE
2) Painless genital Papule becoming a BEEFY-RED ULCER with a characterstic rolled edge
of granulation tissue having raised lesion with white border, 1 or multiple in
number GRANULOMA INGUINALE.. Caused by Klebsiella granulomatis..
Dx: Touch Biopsy will show DONOVAN BODIES.Rx: DOXYCYCLINE or
AZITHROMYCIN.
3) Painful penile, vulvar or cervical vesicle with ulcer with inguinal lymphadenopathy,
ulcer
is
regular,
red,
shallow.,
multiple
in
number
GENITAL
HERPES.associated with Malaise, myalgias, fever with genital burning and
pruritis.. Dx: Tzank smear shows multinucleated giant cells, viral cultures, DFA
serology. Rx: Acyclovir, Famciclovir or valacyclovir.

INFECTIOUS DISEASES
1) Acute diarrhea <2 weeks; Chronic diarrhea >2 weeks (non-infectious), Persistant
diarrhea >2 weeks (infectious)
2) In any case of diarrhea; 1st rule out Infectious cause by history and stool test
Watery diarrhea
History
Stool
Treatment
Bacillus cerueus
Eemtic: Abrupt onset of nausea and
vomiting 1-6 hour after eating
Reheated rice esp from Chinese
restaurant (Heat stable toxin)

Cryptosporidium

Isospora
Giardia

Diarrheal: Abdominal cramps and

watery diarrhea 6-14 hours after
eating vegetable, sauce or pouding
(Heat labile toxin)
AIDS patients with CD-4 <180
i)
Modified
acid
fast
stain shows
oocytes
in
stool.
ii) Duodenal
biopsy
can
also be done

i) HAART
ii) Nitrozxide or
Paromomycin
iii) Boiled water

Abdominal fullness, bloating, gas, Adhesive disk Metronidazole

malabsorption, foul smelling stool, stool
after consuming unfiltered water in examination

Staphlococcus
aureus
Vibro vulnificus

Vibrio
parahemolyticus
BLOODY DIARRHEA
Salmonella
Shigella
Yersenia
Campylobacter

camps, trips or fresh mountain

streams
Abrupt onset of diarrhea within 1-6
hours after eating eggs, salad, eat,
myonnes or custard
Contaminated seafood esp in
patients
with
CLD
or
Hemachromatosis. It also causes
wound infection
Contaminated seafood in patients
with CLD.
History
Egg, chicken
Mimics appendicitis; esp in patients
with
iron
overload(hemochromatosis)
Most common cause of bacterial
gastroenteritis and bloody diarrhea.
Also causing reactive arthritis and
GBS
Eating hamburger giving HUS

Enterohemorrhagic
E.coli (o157:H7)
Pseudomembranous Recent use of antibiotics esp
colitis (C.difficile)
Clindamycin.
Symptoms
begin
within 1st week or even upto 6
weeks with abdominal pain,
diarrhea(bloody/watery)

Stool

Treatment

S
shape
growth at 42
degree
calsius

i)
Stool
culture
ii) Toxin A,B
detection has
greater
specificity
using ELISA

Oral Metro..> if
recur..> Again
Metro..> if no
response> Oral
vanco
If severe: IVIg

3) AIDS patient with multiple RING ENHANCING LESIONS ON CT-SCAN with CD4<100 =
TOXOPLASMOSIS..Rx: Sulfadiazine + Pyrimethamine+Folinic acid for 6 weeks (If
sulfa allergy = use Clindamycin).. If mass effect: Use steroids
Note: i) For prophylaxis of Toxo = CO-TRIMOXAZOLE (Trimethoprim+Sulfamethoxazole)
ii) If any AIDS patient comes with ring enhancing lesion on CT.. there are 2
possibilities either TOXOPLOSMOSIS or CNS LYMPHOMA but you should start on
Sulfadiazine and Pyrimethamine for 2 weeks and repeat CT. the purpose of therapy here
is both diagnostic and therapeutic eg: if after 2 weeks the lesion is not regressing= think
of Lymphoma. (

4) Patient from Northeast (Connecticut, New York, New-jersy, Massachusetts, Wisconsin,

Maryland, Pennsylvania, Delaware, Rhode island) with history of Tick bite and flu like
symptoms with Rash not associated with itching or burning but expanding erythematous
with central clearing (Erythema migrans/ BULLS EYE RASH) = LYME DISEASE= caused
by Borrelia burgdorferi and transmitted by Ixodes tick (deer tick) (also vector for
Babesia)Dx: ELISA, Westrn blot (confirmatory) Rx: Doxycycline, Ceftriaxone.if
pregnant/<9year child (Amoxicillin for 21 days) Advise patient not to DONATE
BLOOD. And say that this disease is rarely if fatal.
For stage2 and 3 (IV ceftriaxone/ penicillin).
Dx tests are done if the diagnosis is suspicious and there is no history of Tick bite=
Quantitative ELISA/WESTERN BLOT
Stages:
i) Early localized: Erythema chronicum migrans (Bulls eye/target lesion >10cm) rash
goes away within 2 weeks.
ii) Early dissiminated: Neurologic (bells palsy), Cardiac (AV nodal block)
iii) Late dissiminated: Chronic monoarthritis, Migratory arthritis.. affects large joints esp
Knees. (Intermittent inflammatory arthritis is typical presentation)
60% untreated will develop joint arthritis
(BAKE a Key Lyme pie: Bells palsy, Arthritis, Kardiac, Erythema migrans)
Asymptomatic tick bite
Rash
Joint, 7th nerve (2nd n 3rd stage)
Cardiac/ Neurologic (2ND N 3RD)
Dil aur dimagh k lea i/v cef deni ha

No treatment done
Doxycycline /Amoxicillin in (pregnant, bachy,
lactating
Doxycycline/ Amoxicillin/ Cefuroxime/
I/v ceftriaxone

For tick to transmit the disease; it must be attached atleast >24 hours to the
body (v.v.v.v..v.vimp)
If it is found attached, Remove the tick with Twizer with the firmly attaching as close to
skin as possible
5) A patient with history of Tick bite, flu like symptoms WITHOUT ANY RASH, but with
Leukopenia/ Thrombocytopenia and Elevated liver enzymes = EHRLICHIOSIS.
Caused by Ehrlichia .. Also known as Spot less Rocks mountain spotted fever
Immediately start treatment with DOXYCYCLINE..
Note: Peripheral blood smear may show Interacellular inclusions (Morulae) in WBc
(v.imp mcq).

Tick bite+No rash+Leukopenia+thrombocytopenia+Elevated liver enzymes = Erlichia

Tick bite (dermacenter) + Influenza like + Centripetal rash= Rocky mountain spotted
feverDx: Weil felix. Rickettsia can affect endothelial lining cause the widespread
vasculitic necrosis of brain, liver, kidney, lung, git leading to GIT pain, edema due to
proteinuria, arthralgias, conjunctivitis. Prevalent in east-coast mountain areas during
spring/summer seasons Rx: DOXYCYCLINE,
If preg: Chloramphenicol
FLASHCARD=67
6) An AIDS patient with chronic pulmonary infection, Hepatosplenomegaly,
Mucocutaneous (tongue, palate) ULCERS = HISTOPLASMOSIS (invades
reticuloendothelial cells and causes HSM and pancytopenia) Endemic in East Lakes,
Ohio, Mississipi, Missouri Comes from exposure to BIRD OR BAT EXCRETA.
Note: Can also occur in normal patients exposed to bird or bad excreta or ppl doing cave
exploration, bulldozing starling roots causing Acute pulmonary infections and as it goes
into reticuloendothelial systems so can cause HEPATOSPLENOMEGALY. The lesions it
forms may calcify with time.. DYSTROPHIC CALCIFICATION IN SPLEENRx:
Amphotericin followed by life long Itraconazole
Diagnosed by: Urine and serum polysaccharide antigen test (most sensitive for making
initial dx of dissiminated disease, monitoring response to therapy and diagnosing relapse)
Best initial test : Histoplasmosis urine antigen
Most accurate: Biopsy with culture
7)
Histoplasmosis
Tissue form: Small intercellular yeast
with a narrow neck
Facultative intracellular parasite in
reticuloendothelial system
Associated with Bat and Bird excreta
(EG. In cave exploers)
Normal patients: acute pulmonary
Imm.Comp: chronic pul/ dissiminated

Blastomycosis (Blasto Buds

Broadly and cause Bony lesion)
Tissue form: Broad based budding
yeast with a double refractile cell
wall
Associated with contact with soil or
rotting wood in Ohio, Missipisi,
Wisconian)
Normal patients: Acute pul
Imm.Comp:
chronic
pul/dissiminated
Bone, Skin, Prostate, Joints, Lungs
Skin: Verocus, Ulcerative

Coccidoies
Only dimorphic fungus which is
SPHERULES in tissue (not yeast)

Southwest U.S . cases increase

after earthquake b/c spherules
thrown up in air
Normal
pts:
Erythema
nodosum(desert
bumps)
also
arthralgias
and
erythema
multiforme/
self
resolving
pneumonia(valley fever)
Imm.comp: Calcifying chronic
pul/dissiminated/ military pattern
on chest x-ray
Preg: 3rd trimester dissiminated

Chest X-Ray: Hilar lymphadenopathy

with or without pneumonitis
AIDS pts have Ulcers on mucous
membranes and mouth
Most common ocular involvement =
RETINA

Chest X-ray: Multiple nodules or

dense consolidation
Not common in AIDS but other
patients may have Ulcerative or
verrocous skin lesions, Plaque
like lesions on mucous membrane,
Osteolytic bone lesions and prostate
involvement

Rx with Amphotericin B

Skin lesions in blastomycosis: start

as pimple and then become verrocus
and ulcerated (flashcard=114)
i)
verrocus:
initiallay
papulopustularcrusted heaped
up and warty..violaceous hue,
sharp borders.. may have abscess
Rx: Itra and Amphotericin B
Note Buzz words:
i) River valleys (Ohio, Missisipi), Wet, Bird , oral and palatal ulcers = Histoplasmosis.Rx:
Amphotericinand in AIDS patients IV AMPHOTERICIN B followed by LIFELONE TREATMENT
WITH ITRACONAZOLE
ii) Dry, Deserts, involving joints, pleuritic chest pain, Erythema nodosum = Coccidiomycosis..Rx:
Amhpotericin
iii) Broad budding yest in decaying organic matter (woods), giving Bone lesions = Blastomycosis..Rx:
Amphotericin

7) A Gardner with a non tender nodule/papule on the site of trauma which later ulcerates;
some secondary subcutaneous nodules along lymphatic tracts which also ulcerate =
SPOROTRICHOSIS
Cause:
Sporothrix schenckii is a DIMORPHIC FUNGI i) Hyphae (branched rossete shaped) at 25
oc
ii) Cigar shaped budding yeast (at 37). It resides in soil, plants, bark of trees,
shrubs, garden plant-invades by rose thorn prick subcutaneously and travel along
lymphatics without giving LYMPHADENOPATHY or SYSTEMIC SIGNS but forms
MULTIPLE SUBCUTANEOUS NODULES.
Rx: Oral POTASSIUM IODIDE, Antifungal (for extracutaneous involvement) =
Amphotericin B, Itraconazole
8) Diseases caused by Pseudomonas (PSEUDO) =gram negative rod
i) Pneumonia
a) Esp in Cystic fibrosis patients, CGD, Neutropenic,
Ventilator patients
b) In cystic fibrosis patients = always high slime producing
strains
c) Nosocomial pneumonia:

ii) Septicemia and Skin

(v.imp MCQ)

Fever, shock, skin lesion (Black necrotic center with

erythematous margin) = ECTHYMA GANGRENOSUM. (pic
given in mcq v,v,v,imp)
Note: septecimia is also common in neutropenic and CGD
patients also in Burn patients (SKIN-Escharcellulitis with blue green pus-septecemia
iii) External otitis
Swimmers ear, Malignant otitis externa doc: I/V
CIPROFLOXACIN () NO SURGICAL DEBRIBEMENT NEEDED
iv) UTI
In catheterized patients
v) Osteomyelitis
Puncture wound esp with rubber shoes and in Diabetic
patients (v.v.v.v.imp mcq)
Note: i) Pseudomonas is a ubiquitous water and soil organism and is found in Raw
vegetebles, Humidifiers, sink drains, Watered bouquet, whirlpools, flowers
ii) No flower or raw vegetables should be taken to burn units
iii) Pseudomonas is gram negative rod, aerobic, oxidase positive (AEROGNOSIA =
AEROBE)
iv) Endotoxin causes inflammation and septicemia and exotoxin A causes ADP
ribosylation of Eef-2 and inactivates it so protein synthesis is inhibited esp in liver. Its
slime layer and capsule make it difficult to be removed from phagocytes
9) Lung cavity with dissiminated lung infection(subacute pneumonia, nodules, cavities
etc) in Immunocompromised patients (AIDS, Lymphoma, Organ transplant), Smear
showing BRANCHING PARTIALLY GRAM POSITIVE FILAMENTOUS RODS(Crooked,
branching, beaded) WITH WEAK ACID FAST STAINING = NOCARDIA. Best initial
test=x-ray, most accurate=culture..Rx: TMP-SMX (D.O.C)best oral alternative:
Minocycline v.v.v.imp mcq. Nocardia produces granulomatous microabscesses
in lung Dissiminated disease may cause subcutaneous or brain abscess ( 50% pts
present with extrapulmonary dissemination with brain being the most common It is just
like T.B the only difference which will be found on scenario is PARTIALLY ACID FAST
FILAMENTOUS ROD

10) A patient with history of dental/facial trauma/diabetic with slowely progressive nontender indurated mass which evolvs into multiple abscess, fistulae and draining sinus with
sulfur granules in Cervical, Abdominal and Thoracic region, Staining shows BRANCHING
PARTIALLY GRAM POSITIVE FILAMENTOUS RODS WITH no ACID FAST STAINING =
ACTINOMYCES..Confirmatory: Anaerobic culture Rx: High dose penicillin for 612 weeks. V.v.v.v.imp mcq
Note: Nocardia is aerobe so it causes infection in Lung whereas Actinomyces is anaerobe
so no lung infection.
11) Pneumonia: CAP, Nosocomial, Aspiration
CAP:
Typical
1) Lobar(strep.pneumo mcc)
2) Broncho:
Staph (esp after flu and cystic fib,
IVDA)
H.influenza (CPOD bronchiectasis)

Atypical
Mycoplasma (young, healthy pts)
Chlamydia (hoarsness causes)
Leigonella

Klebsilla (alcoholic, diabetic)

Some special assocaitions of pneumonia with organisms:

Leigonella

i) Comes from air-conditioners,

ventilators, cruise ships, cooling
(travel
towers
associated
ii) Abdominal pain, diarrhea,
from
cruise confusion, headache
ships)
iii) Causes destruction of JG
apparatus leading to decreased
aldosterone and lab findings of
Addison along with type-4 RTA

Best screening test:

Urine antigen
Culture: Charcol yeast
Rx: Azithromycin or
Fluoroquinolone

Staphylococcus i) yellow sputum

Rx: TMP-SMX
ii) Superimposed on influenza
pneumonia
and
measles IVDA, nursing home,
pneumonia
nosocomial,
Cystic
fibrosis,
Recent
influenza infection

iii) Major lung pathogen in cystic

fibrosis and IVDA
Gram positive cocci in
iv)
Causes
Hemorrhagic clusters
pulmonary edema, Multiple lung
abscesses,
Tension
pneumatoceles
which
may
rupture
to
give
tension
pneumothorax
Drug of choice for aspiration pneumonia = Clindamycin

12)UTI
Cystitis
Honeymoon
cystitis: Due
to
sexual
intercourse
and massage
on
urethra,
bacteria
go
up and cause
cystitis
ASCENDING
INFECTION

Frequency, Urgency, Burning, Best initial test: Urianalysis

dysuria, pus cells in urine+
Suprapubic tenderness
Most accurate: Urine culture
Best
initial
step
in
management after doing
urianalysis= start treatment if
diagnosis is clear on history
and physical examination (uw
Rx:
i) Uncomplicated = TMP-SMX
for 3 days (v.imp mcq)
but if E.coli resistance >20%
= Cipro/Levo
ii) Complicated: TMP-SMX for
7 days or Ciprofloxacin

Pyelonephritis Frequency, Urgency, Burning,

dysuria + Flank pain and
tenderness+ High Fever and pus
(If you have cells in urine
started
empiric
Best initial test: Urinanalysis
treatment
Most accurate: Urine culture
and obtained

Outpatinet: Ciprofloxacin
1st draw blood and urine
cultures and start empiric
antibiotics (vimp
Inpatient:
Ampicillin/Gentamicin

a culture then
after result of
culture can
shift to oral
therapy eg:
TMP-SMX for
2 weeks

Or any gram-ve drug eg

Ceftriaxone
For 2 weeks
If multidrug resistant =
Aminoglycosiedes used
See
Diagnostic
tst
flashcard=72

If a patient of pyelonephritis is treated and does not responds to treatment after

2-3 days and still fever with pus cells in urine = PERINEPHRIC ABSCESS
Perform USG or CT to find the collection.. Biopsy (most accurate) Rx:
Quinolone + Staphylococcal coverage.. (Jinay vi respond ni kita oodi anatomy nu
check kro by USG)

Uncomplicated cystitis in females

(
Cystitis in diabetes
Cystitis in male
Cystitis in pregnancy/
Asymptomatic bacteria

3 days course of TMP-SMX or quinolone or

Nitrofurantion
TMP-SMX for 7 days
10-14 days TMP-SMX or quinolone
10-14 days course of Nitrofurantoin,
amoxicillin or macrodantin
Nitrofurantion for 7 days

UTI in indwelling catheter patients with alkaline urine = Proteus

Note: If a sexually active lady comes to you with c/f of cystitis. Next step: do BETA HCG
n urianlysis. If pregnancy test negative and u.a is positive. Give tmp-smx for 3
days but if beta hcg comes positive.. give nitrofurantoin for 7 days and meanwhile
order urine culture and repeat it after 2 weeks to ensure the eradication of bacteria.
(v.v.imp ccs case)

13) A patient with painful localized rash with vesicles and papules eg on Hands
along with regional localized painful lymphadenopathy which may be suppurative
= CAT-SCRATCH DISEASE.. Caused by Bartonella hensale (cat bite, flea bite,
cat scratch)s..Rx: Oral Azithromycin for 5 days

14) Single stranded ve RNA viruses: Pain Results From Our Bunions Always.

Paramyxo, Rhabdo, Flivo, Orthomyxo, Bunya, Arena (all are enveloped)

Ortho is odd: It is linear RNA but 8 segments, it replicates in both cytoplasm
and nucleus. All others replicate in cytoplasm.
15) Orthomyxovirus: Influenza A= birds, pigs, human
B=only human
Envelope contains: Hemagluttinin (promotes viral entry) and Neuraminidase
(promotes progeny virion release)..
Look for a patient with arthralgia, myalgia, cough, headache, fever, sore
throat, tiredness. Next best step: Viral antigen detection on
nasopharyngeal swab (if patient has come <48 hours).. Labs may
show Leukopenia and Proteinuria Cxray may be normal or may show
interstitial or alveolar pattern
Rx:
If patient presents <48 hours = Oseltamivir / Zanamavir (neuraminidase
inhibitors work against both A and B)
If >48 hours = Bed rest and acetaminophen only
Note:
i) Amantadine and Rimantadine are only effective against influenza A
ii) Osealtamivir is given orally while zanamavir is inhaled.
iii) Indications of Influenza vaccine: COPD, CHF, Dialysis patients, Steroid
use, patients undergoing chemotherapy, Immunocompromised, Health care
workers, everyone >50, AIDS patients at any Tcell count grreatr>200 (uw),
Pregnant women, Cystic fibrosis
iv) Yellow In Egg: Yellow fever and Influenza vaccine are contra-indicated
in Egg allergy.
v) Genetic Shift: Reassortment of viral genome (causes severe pandemic)
vi) Genetic Drift: Minor changes based on random mutation (causes
epidemic)
vii) Do not give influenza vaccine <6 months of age
viii) Jo indications pneumococcal ki hain wohe influenza vaccine ki bi hain except: INFLUENZA IS ONLY GIVEN TO
PREGNANT WOMEN AND HEALTHCARE WORKERS
IX) EVERYONE >50 = influenza vaccine annualy

x) Everyone >65 = Pneumococcal vaccine Once only (but agar 65 se pehly bi koi dose mila ha to 65 pe lazmi dobara
dena hoga)..Conrad Fischer Case on Pneumonia (v.v.v.v.v.imp)
Pneumococcal <65: cardiovascular, pulmonary, hepatic, renal, metabolic (dm), alcoholism, csf leaks, cochlear imlants,
immunosupreesion, cigerate smoking,, cLD, CHF, CKD, COPD, asthma

Live influenze
Intranasal
C.I in immunocompromised, >50years, pregnancy,
patients undergoing chemo, egg allergy
>2-49 years of age to pts who are Non pregnant and
immunocompetent

Inactivated influenza
I/M
Egg allergy
Annualy given to everyone in Flu season >6 months of
age

16) Listeria monocytogenes: Gram positive rod with endotoxin, forms actin rockets
and move cell to cell; characterstics tumbling motility. Acquired by ingestion of
UNPASTEURIZED MILK/ CHEESE, deli meats or by vaginal transmission during
childbirth
1) Pregnancy
Last trimester; febrile illness;gastro;
amnionitis (MURKY BROWN FLUID);
SPONTANOUS ABORTION
2) Granulomatosis infantisepticum
Dissiminated abscesses, granulomas
3) Bacteremia
Neonates/ immunocompromised
4) Meningitis
Neonates; adults; immunocompromised;
HIV.
CSF
shows
neutrophilic
pleocytosis
17) Botulism
Adult
Food poisoning
Heat labile toxin released in Canned
foods and ingested

Infant
Floppy baby syndrome
Spores found in Honey and after
ingestion; spores produce toxin into
large intestine
Toxin is absorbed slowely from large
intestine over days and then blocks
acetylcholine release

Toxin spreads via blood into peripheral

cholinergic
fibers
and
blocks
acetylcholine release within 12-36
hours
Cranial nerves (Diplopia, dysarthria, Constipation and flaccid paralysis
dysphagia, ptosis)
NM junction: Symmetrical desending
paralysis

Postganglionic parasympathic
(dizziness, dry throat, ptosis)

fibers

18) Mumps causes painful enlargment of parotid glands; redness and swelling of stenson ducts; causes edema of soft
palate, larynx and even UPPER CHEST...... Dx by Lymphocytosis, Inc . Amylase, IgM and IgG.... Complications include
MENINGIOENCEPHLITIS, EPIDIDYMO-ORCHITIS, PANCREATITIS, DEAFNESS.....
Meningitis can occur along with parotitis or after 10 days of parotitis.... ORCHITIS is seen in POST-PUBERTAL MALES
not pre-pubertal....................
If mumps to fetus in intra-uterine life = leads to SUBENDOCARDIAL FIBROELASTOSIS
Mumps is characterized by:
Incubation period: 15-24 days
Mild prodromal signs: malaise, low grade fever, headache, myalgias, anorexia
Parotitis is present in 95% patients and 80% bilateral.
Orchitis is the most common complication (30% bilateral) and is most common is post-pubertal males. It presents as
an abrupt onset of fever, testicular pain and swelling of scrotum, and is treated with NSAID, bed rest and local cooling
measures. (
Orchitis, Aseptic meningitis, meningoencephlitis

RHEUMATOLOGY/ MUSCULOSKELETAL
1) A 20-50 year woman with chronic widespread pain, not relieved by NSAID,
fatigue, poor sleep, irritable bowel, 11/18 trigger point tenderness or multiple
symmetrically distributed tender spots over muscles, joints, tendons, symptoms
worse in morning but exacerbated with exercise, with all labs normal (ESR etc) =
FIBROMYALGIA. Associated with Irritable bladder, IBS, headache, TMJ pain.
Rx: Exercise and Tricyclic antidepressants These women are at increased risk
for PANIC DISORDER.(NBME BLOCK3-QUESTION 5)
2) A young patient or child with wasting and weakness of facial muscles and
muscles of distal limbs, Myotonia (inability to relax contracted muscles patient
hath pakar k chor nai skta), upper lip in inverted V shape, Frontal Baldness,
Testicular atrophy, decreased glucose tolerance (DM), Hypothyroidism, Cataracts
= MYOTONIC DYSTROPHY/ Steinert disease. AUTOSOMAL DOMINANAT

resulting in increased CTG repeats in the myotonin protein kinase on

chromosome 19All the muscles are involved SMOOTH, SKELETAL,
CARDIAC..Rx: Phenytoin
Endocrine
Nervous

Immunologic
Cardiac

DM, Hypothyroidism, Testicular

atrophy
Emaciated extremeties, wasting of
thenar and hypothenar, winged
scapula, myotony
Conduction defects

Note: trinucleotide repeat expansion diseases (Try Hunting for My Fried eggs X)
i) Huntington = CAG
ii) MyoTonic = CTG
iii) FraGile X syndrome = CGG
iv) Fredrisch Ataxia= GAA
These disesases may show phenomena of GENETIC ANTICIPATION= disease
severity increases and age of onset decreases in successive generations b/c of
increase in number of repeats. (
Note: Anabolic steroids used by bodybuilders can also lead to testicular atrophy.
As exogenous testosterone analogue causes feedback inhibition of GnRH which
leads to decreased FSH and LH (FSH AND LH ARE TROPHIC FOR TESTIS). So
testicular atrophy and azospermia happens. Other adverse effects of anabolic
steroids are:
Acne, Erythrocytosis, Gynacomastia, Cholestasis, Hepatic failure, Dyslipidemia,
Behavioual effects (aggressiveness, psychosis

3) A patient with proximal muscle weakness + skin rash = DERMATOMYOSITIS..

Best initial test: CPK and Aldolase levels.. Confirmatory test= Muscle
biopsy
C.F: Proximal muscle weakness (difficulty getting up from seated position/ walking
up stairs), 1/4th have pain and tenderness, dysphagia/difficult to initiate
swallowing b/c of involvement of striated muscles of pharynx.
Patients may also develop MYOCARDITIS and CARDIAC CONDUCTION defects
Skin changes: Malar rash, Heliotrope rash, Gottron papules.. 25% associated
with cancers (ovary, lung, GIT, Lymphoma, Breast)
ANA is positive but non-specific, Anti-Jo antibodies are associated with Lung
fibrosis.. Muscle Fibers are involved b/c of inflammation, necrosis, fiber
atrophy or Antibody-mediated damage. Proximal muscles are involved
symmetrically
Rx: Steroids. Methotrexate/Azathioprine/ IvIg/ Mycophenolate.
Hydroxychloroquine for Skin.
Note:
i) Dermato/polymyositis = Muscle fibers are involved
ii) Lambert-Eaton = Presynaptic membrane is damaged (calcium channals); weakness
improves with use

iii) Myasthenia gravis= Postsynaptic membrane(cholinergic receptors) is damaged; weakness

aggravate with use

NEUROLOGY
1) In all patients with suspected stroke = DO CT SCAN WITHOUT CONTRAST to
rule out hemorrhagic stroke..and if found ischemic stroke = give T-PA
witin 4.5 hours. Hypertension should only be treated if systolic >220 or
diastolic >130 mmHg.
2)
Types of Lacunar Infarcts (Main causes = Diabetes and Hypertension)
Pure sensory stroke
v.imp MCQ)

VPL nucleus of thalamus

VPM nucleus of
thalamus

Pure Motor hemiparesis

Ataxic-hemiparesis

Posterior limb of I.C

Posterior limb of I.C

Visible Panty Lines (VPL)

Sensory loss of
contralateral body (VPL)
Contralateral face (VPM)

Dysarthria clumsy hand

syndrome

Basis pontis

Hand weakness, Mild

motor aphasia, NO
sensory abnormalities

2) Alcoholic patient with triad of ENCEPHLOPATHY, OCCULOMOTOR

DYSFUNCTION, GAIT ATAXIA = WERNIKE-KORASAKOFF SYNDROME
Thiamine deficiency in Alcoholic leading to ATROPHY OF MAMILLARY BODIES.
Note: Chronic Thiamine deficiency leads to Korasakofffs dyndrome characterized
by IRREVERSIBLE AMNESIA, CONFABULATION & APATHY

2) A patient with progressive ascending paralysis, some parasthesias and tingling

in legs, some autonomic dysfunction (sweating, postural hypotension, labile BP) =
GULLIAN BARRIE SYNDROME.. Most common precipitating organism =
CAMPYLOBACTER JEJUNI (V.IMP MCQ).. In later stages it may involve Bilateral
Facial nerve and in 5% patients death happens due to respiratory
paralysis.(diaphragm involvement). ()
CSF will show ALBUMINOCYTOLOGICAL DISSOCIATION (but CSF may be normal in
1st 10 days) The most specific diagnostic test = NERVE CONDUCTION
STUDIES/ELECTROMYOGRAPHY.
What test is done for respiratory muscle involvement/ the most urgent step:
FORCED VITAL CAPACITY./ PULMONARY FUNCTION TESTS..
RX: IvIg or Plasmapheresis. (do not combine IVIg with plasmapheresis)

3) An obese female on OCP/steroids/vitamin A; with headache that is suggestive of brain

tumor but with normal CT/MRI and elevated CSF pressure = PSEUDOTUMOR CEREBRI
(Benign intracranial hypertension). c/f: There are no focal neurological deficiets
except for 6th nerve palsy, Papilledema and diplopia.The pathology involves impaired
absorption of CSF by Arachnoid villi.. Most deveastating complication: BLINDNESS

4) Rx: Weight loss if fails Acetazolamide. If fails.. Shunting/Optic nerve

sheath fenestration
Note: Sometimes MRI shows empty sella in P.C b.c of downward herniation of arachnocele.

4) DEMENTIA (MMSE = <24)

REVERSIBLE

Type

i)
Hypothyroidism
ii)
ii) B12 deficency
iii) Hepatic encephalopathy
iv) CNS vasculitis
v) Syphilis
vi) Brain abscess
vii) Tumor
viii) Medications (anticholinergics)
ix) Central/ Obs sleep apnea
x) Trauma/ Subdural hematoma
xi) Normal Pressure Hydrocephalus (Gait disturbance,
Dementia, Urinary incontinence) MRI = enlarged
ventricles out of proportion to sulcul atrophy b/c of
diminished absorption of CSF (203). CSF = 1st there is
transient increased in pressure which leads to
enlargement of ventricles but later pressures come to
normal .. .Rx: Shunt placement uw.
GAIT IN NPH= Magnetic/ Feet glued to floor/ broad based
shuffling . Demantia is very slowly progressive.. Later
fecal incontinence may develop..
Rx: 1st do repeated large volume LP> if patient
responds.> then do VP shunt ()
Time course

Alzhimer disase
Gradual
>60 years
(Dementia presents Pathophysiolgy
with progressive

Pathology

C/F and
imaging
Diffuse atrophy i) Amnesia-
with enlarged
Language
ventricles, senile deficitplaques and
acalculia-

memory
disturbances(shortLong),
disorientation,
aphasia,
visuospatial
deficits, loss of
motor skills or
incontinence)
Most of the cases,
Long term memory
is preserved
Clue: Gradually
progressive
memory loss with
one or more of
following: Apraxia,
agnosia, aphasia,
or disturbed
executive
function then
hypersexuality may
happen .Ye log
aksar rasta bhool
jaty hain
Picks disease
(just like Alzhmier
but women > men
and 40-60 years)

a) DECREASED
ACETYLCHOLINE
(Degeneration of
nucleus of Meyenret)
b) Def of choline
acetyltransferase
c) Abnormal amyloid
gene expression
Treatment:
i) Donepezil (slows
progression)
ii) Memantine (NMDA
antagonist)
iii) Resperidone to
decrease agitation

neurofibrillary
tangles(
intracellular
composed of
tau protein),
neuritic plaques,
amyloid
angiopathy,
Hairano bodies
in hippocampus,
granulovacuolar
degeneration

depressionagitation
and psychosis
ii) Mild
cognitive
impairment
iii) Cause of
death =
Aspiration
pneumonia
CT: diffuse
cortical and
subcortical
atrophy

(alpha helix transforms

into beta pleated
sheath which forms
aggregates of beta
amyloid extracellualar)
Amyloid angiopathy
causes multiple
intracerebral bleed

Gradual

(Less memory loss but

more personality
changes-/
Personality changes COMPULSIVE
with sparing of
BEHAVIOUR
visuo-spatial
Eventually profound
functions
dementia and become

Pick bodies
(round
intraneuronal
inclusions of tau
protein with
silver stain)
v.v.v.imp MCQ,,
Cortical atrophy
of FrontoTemporal lobes

SYMMETRICA
L FRONTOTEMPORAL
ATROPHY
/Frontal lobe
gliosis on
MRI/CT

mute, immotile,
incontinent
(Featues of Kluver
busy
syndrome=hypephagia
, hypersexuality)
Lewy body
dementia/Parkinso
n

Fluctuating cognitive
impairment +
hallucinations

A 72-year-old retired
surgeon develops
progressive cognitive
decline over one year.
He also experiences
occasional visual
hallucinations, poor
attention, short-term
memory loss, and
bilateral upper extremity
rigidity.

Binswanger disease
Vascular dementia Abrupt
(male>woman)
Hypetensive,
Evidence of focal signs
diabetic, CVA
Faster deterioration
than Alzhmier (stepwise and patchy
deterioration)

Eosinophilic
CYTOPLASmic
inclusion bodies
in nerve cells

Rx is same as for
Alzhmier (

Multiple areas
of increased T-2
weighted
density in
periventricular
areas
(hyperedense(

It is the second
most common
form of
degenerative
dementia next to
Alzheimers
dementia,
accounting for as
much as 20% of
cases in the
elderly. In
addition to
dementia, the
disease is
characterized by
extrapyramidal
signs (rigidity)
that are
reminiscent of
Parkinsons
disease. Patients
also can
experience
psychosis (visual
hallucinations).

Evidence of
old infarctions
or extensive
deep whitematter
changes
secondary to
chronic
ischemia

Creutzfeldt-Jakob
disease (CJD)

Abrupt
(Rapidly progressive
dementia with
MyocloniWc jerks)

Prions protein
on brain
biopsy(most
accurate test)
CSF=14-3-3
PROTEIN
Spongiform
changes on
biopsy
Spongiform
encephlpathy

Pseudodementia
(

Just like AD but

PATIENT IS ACTIVELY
CONCERNED ABOUT
MEMORY LOSS

Huntington Disease Autosomal dominant

with complete
(Hunt = 4)
penetrance.
CAG trinucleotide
repeat on
chromosome 4 on HD
CT SCAN: Caudate
gene that codes for
atrophy with
protein Huntingtin.
This protein decreases

Depression in
adults can also
present as
pseudodementi
a
Triad of
i) Movement
disorder
(Dyskinesia,
ataxia, Facial
grimacing,
dystonia,
tongue
movements

MRI with
diffusion
weighted may
show
increased T2
and FLAIR
intensity in
putamen and
head of
caudate.
EEG:
Pyramidal
signs and
periodic
sharp waves
(mcq)/
Synchronous
Triphasic /
BIPHASIC
spikes and
waves
Rx: SSRI

Striatal
degeneration
Rx:
i) Dyskinesia =
Tetrabenazine
ii) Psychosis =
Haloperidol

ventricular
enlargment

Note:
Acetylation
enhances gene
transcription while
Methylation
decreases the gene
transcription (u.w
online MCQ)

the expression of
other genes by
inhibiting their
transcription called
TRANSCRIPTIOAL
REPRESSION/
SILENCING . This
repression is due to
HYPERMETHYLATION
OF HISTONES(v.imp
mcq)
DECREASED
ACETYLCHOLINE AND
DECREASED GABA

choreform
movements)
ii) Memory
(Dementia)..
Late finding
iii) Behaviour
(moodiness,
irritability,
antisocial,
psychosis,
suicidal,
cognitive
decline
flashcard=249)

Note:
In normal aging, patient remains functional, does his work, may forget something
(broca aphasia) but still is social and can drive but patients with dementia are
functionally impaired and often rasta bhool jaty hain. (
Nomal aging: tiredness, occasional forgetfulness, occasional word finding
difficullty, trouble falling asleep, no functional impairment..
Functional impairment = dementia ()
Alzhmier=Ghajni wala amir khan (wo movie k start me he get lost hojatata tha in
neighbourhood aur usy short term memory loss bi tha. Baad me uy gait
impairment howi the)
Key points
Alzhmier
(

Early changes
i) Visuospatial (getting lost
in neighbourhood)

Late changes
i) Personality and
behavior
(hypersexuality)

Pathology

ii) Anterograde amnesia

(old memories are
preseverd = Ghajni wala
amir khan)
iii) Apraxia

Lewy
body

NPH

i) Visual hallucinations
ii) Alertness alteration
iii) Extrapyrimidal
iv) Fluctuating cognitive
impairment

Gait and urinary

incontinence

ii) Hallucinations
iii) Change in
alertness
iv) Gait impairment
and urinary
incontinenced
v) Inability to
perform daily
activities (apraxia
etc)/ cognitive
decline
Motor
(Note that in
Parkinson, motor
symptoms are early
and other are late
unlike lewy body
dementia)

Lewy bodies
(eosinophilic
Intracytoplasmic
inclusions of
Alphasynecluein
protein in
substantia
nigra) Mtb-2
page=288)

Memory

5) A patient with Resting tremors+ Rigidity + Bradykinesia = PARKINSONs

diseasePatient has shuffling gait, positive gallabelar tap and monotonous
speech, Positive Retropulsion
i) Parkinson + Vertical gaze palsy = Supranuclear palsy (v.imp mcq)
ii) Parkinson + Ataxia = Olivopontocerebellar atrophy
iii) Parkinson + Prominent orthostatic hypotension+widespread neurological signs
= Shy dragger syndrome (Multiple system atrophy)
Rx:

i) If mild/ TREMORS, RIGIDITY = Anticholinergic (Benztropine,

Trihexyphenidyl).. If patient >60 and cant tolerate anticholinergics =
AMANTADINE
ii) If severe/ Bradykinesia/ Orthostatic = Best initial = Dopamine agonists
(Pramipexole, Roprinole) Pramipexole also used for RESTLESS LEG SYNDROME
(v.imp mcq)
Levodopa-Carbidopa (most effective) Results in ON-OFF phenomena. For
OFF = give s/c Apomorphine
To extend the duration of Levocabi = comt INHIBITORS (Tolcapone, Entacapone)
Single agent or adjunct to levocarbi = MAO-B inhibitors (Rasagiline, Salagiline)
They are the only WHICH SLOW THE PROGRESSION OF DISEASE (v.imp mcq)
6) A woman with visual disturbances, remitting and relapsing motor and
sensory deficis including spasticity, hyperreflexia = MULTIPLE
SCLEROSIS. Most common clinical presentation = Optic neuritis Most
common physical finding= SPASTICITY Others: Bilateral trigeminal
neuralgia, Internuclear ophthalmoplegia, Charcot triad (Scanning speech,
Nystagmus, Intranuclear ophthalmoplegia)
.Best initial and most accurate test = MRI (shows Dawson bodies with
gadolinium contrast showing oval periventricular plaques in white
matter) If MRI is inconclusive = LUMBUR PUNCTURE (mild elevation
in proteins and WBC & protein electrophoresis shows OLIGOCLONAL IGg
Bands)
Best initial therapy for Acute exacerbation = High dose steroids
Drugs for preventing relapses and remission = B-interferon, Glatiramer
(copolymer-1), Natalizumab, Mitoxantrone, Azathioprine
Drug to delay progression = Mitoxantrone, Natazilumab, Galatimer, Interferon
beta

Natalizumab is a-4 integrin inhibitor which reduces leukocyte migration into CNS
and prevents demyelination
For sasticity = give Baclofen/ Tizanidine
For fatigue = give Amantadine
Patients may develop ATONIC BLADDERRx: Bathenecol
Side effect of Natalizumab is = PROGRESSIVE MULTIFOCAL
LEUKOENCEPHALOPATHY (PML) which shows new multiple white matter
hypodense areas in white matter on MRI. PML is also associated with
papovirus / JC virus and in AIDS patients with CD4<50

7) An IV drug abuser with signs and symptoms of UMN paraplegia = think of

EPIDURAL ABSCESS.. Do immediate MRI of spine

8) Causes of spinal cord compression

Acute
Subacute
Chronic
i) Trauma
i)Neoplasm
i) Disc herniation
Most common site of cord compression = Thoracic segment
Best initial step in cord compression = Steroids
Best initial test for cord compression= X-RAY
Most accurate test = MRI

9) Hand tremors looking like intention tremor but may be present at rest; coarse
in nature; prominent at the end of goal(e.g grasping something) = Benign
Essential tremor Rx: Propranolol or Primidone.

Note: i) Primidone is an anti-convulsant that converts into

Phenylethylmalonamide and phenobarbital. Due to this phenobarbital, it can
precipitate ACUTE INTERMITTENT PORPHYRIA (v.imp mcq)..
10) A patient of Iron deficiency; Chronic kidney disease or Peripheral neuropathy
having discomfort and inability to control the legs at night, relieved by
movements and unpleasant leg sensations = RESTLESS LEG SYNDROME (Ekbom;s
syndrome).. Caused by abnormality in DOPAMINERGIC transmission in
CNS Rx: Dopamine agonists (Roprinole, Pramipexole)..v.imp MCQ
11) A male patient with severe Unilateral Retro-orbital pain that awakens him
from sleep, peaks suddenly and lasts for 2 hours, Associated with Red eyes,
Rhinorrhea, Nasal congestion, Lacrimation and sometimes ipsilateral Horner
syndrome = CLUSTER HEADACHE.......... Immediate Rx: 100% OXYGEN &
subcutaneous sumatriptan.. For prophylaxis: Lithium, steroids, ergometrine

GASTROINTESTINAL

1) A patient with epigastric burning pain radiating upto chest, esp after meals or lying
flat, sore throat, bad taste in mouth, waterbrash, hoarsness, cough = GERD.Best
initial step = start PPI..If diagnosis is unclear = 24 HOUR PH MONITORING (most
sensitive).
Treatment:
i) Mild/intermittent: Liquid antacids or H2 blockers
ii) Persistant / erosive esophagitis = PPI
iii) If not respond to medicl= Nissen fundoplication, Endocinch
Note: i) Do endoscopy if CHRONIC GERD >3 years, signs of obstruction such as
dysphagia/odynophagia, weight loss, anemia or heam positive stools

ii) Barium studies is useless in diagnosis of GERD

IMPORTANT DRUGS
ANTIDEPRESSENTS
Drug
Bupripion
Mirtazapine

Mechanism
NE-Dopamine reuptake
blocker
a-2 antagonist

Use
Smoking cessation
Associated with weight
gain

Note:
i) The two FDA approved medications for nicotine/ smoking cessation are
a) varenicline (partial agonist of nicotine receptors) . Associated with depression
& suicide
b) Buproprion. Norepinephrine dopamine reuptake inhibitor

PULMONOLOGY

1) A patient with sudden onset of chest pain, dyspnea, heart and lungs clear = PULMONARY
EMBOLISM. Proximal DVT is a greater risk factor than distal DVT but (distal DVT is a risk factor
in Pregnancy and upper exterimity DVT)
Investigation of choice = SPIRAL CT/ CT-angiogram.. (but it can miss 15% embolus)
Most sensitive test = D-dimer (only done in low risk patients and in emergency and if it is
negative = send patient to home b/c no embolus)
A patient comes with s/s of P.E:
i) Give Anticoagulation with Heparin
ii) Do Spiral CT--if positive-Rx for PE (Heparin 5-7 days then Warfarin for 6 months)
- If negative (think peripheral embolism).. If low risk pt= do D-DIMER
------------------------------------ ------- If high risk = Doppler USG leg= if negative = Angiogram

Treatment of Pulmonary embolism:

i) if patient hemodynamically stable = Heparin---warfarin (if a.c contraindicated =
do IVC filter)
ii) If patient hemodynamically unstable = 1st give thrombolytic = then same
sequence of heparin and warfarin and similarly if A.C contraindicated = Pulmonary
emolectomy / Interruption of IVC

2) A patient comes with Acute exacerbation of COPD..

Best initial step: Oxygen and ABGs measurement.. then do CHEST-XRAY
And give patient: Albuterol inahlor, Ipratropium, Iv methylpredsinolone,
antibiotics (if fever, sputum or new infiltrate) afte 20 minutesReasses the
patient with ABGS.. suppose ABGs show mild acidosis ie
pH = 7.32
pCo2 = 52
pO2= 60 What to do now? Here do not give patient Oxygen b/c it would
eliminate hypoxic drive start patient on NON-INVASIVE POSITIVE
PRESSURE VENTILATION (CPAP/ BiPAP).. Reassess after 30 minutes if
worsening respiratory acidosis = INTUBATE THE PATIENT
Note:
i) Contraindications of NIPPV: Hypotension, sepsis, Dysrhythmia
ii) Indications of NIPPV: PH <7.35, PCO2 >45, RR >25

TOXICOLOGY
1) Patient comes with headache, confusion, abdominal pain, nausea, vomiting
after spending some time in Basement of some plaza/ Room in a cold night/
confined quarter/smoke inhalation eg from burns/ some indoor place.
Their skin color is pink = CARBONMONOXIDE POISONINGcheck
carboxyhemoglobin levels (most accurate test) and ..Give 100% oxygen

 but if patient has severe symptoms eg CNS and chest pain, metabolic
acidosis = HYPERBARIC OXYGEN at 3atm (
2) Note: i) S/s of toxicity: a) Pulmonary: dyspnea, tachypnea, SOB
b) Neurologic: headache, dizziness, conusion, syncope
c) Cardiac: chest pain, arrhythmia, hypotension
also leads to TYPE-A Lactic acidosis (b/c of poor oxygen delivery to tissue)
ii) CO poisoning initlly presents just like hypoglycemia but fingerstick
glucose is normal. (v.imp)
iii) LABS in CO poisoning:
a)Pulse oximetry = normal b/c CO-Hb is of same color as oxyhb
b) ABG = Metabolic acidosis. pO2 = normal
c) CPK is elevated
2) A person comes after ingestion of pills for suicide/ a patient on treatment of
depression. Presents with 4c { Coma, Convulsions and status epileptics, Cardiac
arrhythmias(v.tachy/ heart block), Cholinergic(anti) = Dry mouth, Tachycardia,
dilated pupil, flushed skin, Hyperthermia, impaired peristalsis} and Hypotension =
TRICYCLIC ANTIDEPRESSANT TOXICITY..
The most common toxicity = Anticholinergic
The most serious toxicity = Cardiac arrhythmia (v.tachy) following prolonged QRS
complex.
The most specific test = Serum drug levels
The most important indicator of severity = Duration of QRS complex (v.imp MCQ)
Rx:
i) secure ABC and Give charcoal in acute setting

ii) If ECG showing QRS prolongation = Give I/V Na-Bicarbonate to narrow down
the QRS complex, improves systolic b.p (v.imp mcq)If non-responsive = give
Lidocaine
nOTE:
i) TCA are non-specific blocker of 5-HT and NE reuptake and their toxicity is due to
Muscrinic blockade, Alpha blockade and Na-channal blockade
ii) Seizure + Arrhythmia + wide QRS after drug ingestion = TCA toxicity
iii) Benzodiazepene prevents the seizure toxicity of TCA. If a patient has taken
both benzo and TCA patient will not develp seizure but when u reverse benzo
with FLUMEZANIL, patient will develop seizure
3) A man comes to emergency after enjoying party with NYSTAGMUS (vertical
and horizontal v.v.v.vimp mcq) + Paranoia + Convulsions + Hallucinations +
agitation + dilated pupils + Hyperthermia+ Hypertension + Muslce rigidity +
rhabdomyolysis +Flushing +impulsivity+ impaied judgment + physical agression =
PHENCYCLIDINE TOXICITY (PCP). Rx with benzodiazepine..
Note: PCP is NMDA-antagonist (v.v.imp mcq as told by Usman nabi)

4) A patient with Respiratory depression, Miosis, bradycardia, depressed mental

status, Decreased bowel sounds, hypothermia, hypotension = OPOID
POISONING Rx: Give I/v Naloxone until respiratory rate increases.. (The
best predictor of opoid poisoning is RESPIRATORY RATE. (v.imp mcq as told by
Asif kamal)
Note:
i) Do not give oxygen to patient b/c opoid cause the blockade of PCo2 sensors in
brain so the respiration is derived now only by baroreceptors which sense hypoxic
drive by PO2.. so giving oxygen will block them too
5) Acid / Alkali burns

Eye

Redness, photophobia,
tearing

Skin

Ingestion

Pain, Odynophagia,
drooling, erythema of
oral cavity, abdominal
pain

1st best step: irrigate

with water until pH
returns to normal
Next: do the thorough
eye examination and if
corneal injury=give
antibiotics
1st best step: bush of
with dry powder and
irrigate with water
1st best step: irrigate
with water and give
patient water to drink
Next: Do ENDOSCOPY
within 24 hours (v.imp
mcq)

Note: i) Do not neutralize these burns

ii) Do not use prophylactic antibiotics
iii) Do not do gastric lavage, do not give corticosteroids or charcoal or do
not pass NG tube but do endoscopy within 24 hours to know the extent of injury.
iv) Common items in history for these burns: Cleaners (dishwasher, oven
cleaner), lye ingestion, hair relaxers

ENDOCRINOLOGY
1) Patient with hearing loss + Increased hat size + Ocassional headache + Failure
to erect the head + Warm skin of head + Kyphosis + Cotton wool appearance on
skull X-RAY = PAGET DISEASE OF BONE associated with Paramyxovirus.
There is impaired remodeling of bone (Osteolytic phase, Mixed phase,
Osteosclerotic phase) M/E shows Mosaic pattern of lamellar bone.. Labs
show Increased Alkaline phosphatase and urine show increased Hydroxyproline
levels..Rx with Bisphosphonates. Complications: High output cardiac
failure, Hearing loss, Chalkstick fracture, Visual disturbances
Note:
Impaired remodeling of bone
Normal mineralization with decreased
mass
Abundant mineralization of
periosteum
Increased osteoid deposition

Fibrous replacement of bone

Pagets disease (v.v.imp MCQ)

Osteoporosis
Hypervitaminosis A
Vitamin D deficiency
Rickets: Defective mineralization of
bone+cartilage
Osteomalacia: Defective mineralization
of bone
Primary hyperparathyroidism

2) AMYLOIDOSIS
Enlarged kidney
B-pleated sheet demonstrable by apple green birefrigrence of Congo red stain
under polarized light; E/M: Extracellular amyloid fibrils. Affected tissue has waxy
appearence

Localized amyloidosis
Single organ
i) Hoarsness (vocal cord)
ii) Propstosis (orbit)
III) carpel tunnel (

Systemic amyloidosis
i) Heart failure (restrictive cmp,
speckled pattern)
ii) Nephrotic syndrome
iii) Autonomic insufficiency
iv) Peripheral neuropathy
v) Waxy rough plaques on skin
vi) Enlarged tongue (macroglossia)
vii) Pseudohypertrophy
Dx: Biopsy from Abdominal fat pad
(v.imp mcq)

Type
Primary
Secondary

Protein
AL (Light chain=L)
AA

Senile cardiac
Type 2 DM
Medullary ca of thyroid
Alzhmier disease
Dialysis associated /
ESRD

Tanserythrin
Amylin
A-CAL
B-amyloid
B-2 microglobulin
(it is not filtered from
dialysis membrane)

Derived from
Ig ligh chains (m.M)
Serum amyloid A
associated protein
(chronic inflammatory
conditions) eg
Rheumatiod arthritis,
psoriasis, ivda, ibd
AF (old Fogies)
AE
Calcitonin
APP
MHC class-1
Mostly leads to Carpal
tunel syndrome

3) Patient with either Eu/Hypo/Hyperthyroid; symmetrically enlarged thyroid with

Firm, Rubbery, Non tender; Positive anti Ts (Thyroglobulin, TPO, TSH receptor) =
HASHIMOTO THYROIDITIS.. Biopsy shows Germinal centers and Hurtle cells..
Association with Autoimmune adrenilitis, TYPE 1 DM,.. Complication= B-CELL
LYMPHOMA OF THYROID (v.imp mcq)

4) A diabetic patient with hyperventilation, altered mental status, Increased anion

gap metabolic acidosis, Non specific abdominal pain, Polydypsia, polyuria =
DIABETIC KETOACIDOSIS. Treat with large volume saline and Insulin
replacement (1st i/v then s/c)
Note:
i) in DKA, although total body potassium is depleted but there is Hyperkalemia in
blood b/c of Intracellular shift and insulin deficiency = this is called Paradoxical
hyperkalemia
ii) Total body potassium is depleted b/c of Increased GIT loss and Osmotic
diuresis. (v.imp mcq)
iii) The most accurate indicator of severity of DKA is SERUM BICARBONATE
levels.(v.imp mcq) ). (Stop treatment when bicarbonates go normal)
iv) As soon as potassium levels fall to 4mEq/L (or it is normal initially on
admission) = Give potassium replacement
v) If glucose goes down = give glucose but dont stop the treatment.. Treatment
should be stopped only when bicarbonates goes up or anion gap normalizes.
5) Hypercalcemia: CHIMPANZEES (Calcium ingestion, Hyperthyroid-parathyroid,
Iatrogenic (thiazide), Multiple myeloma, Pagets disease, Addison disease, Neoplasm,
Zollinger elisson(MEN-1), Excess vit D, excess vitamin A, Sarcoidosis.,. Patients with
Pagets disease are usually normocalcemic but become hypercalcemic if they are
immobilized.
C/F: Stones, bones, groans and psychiatric moans ; confusion, stupor, lethargy,
constipation if hyperparathyroidism (Osteitis fibrosa cystica), constipation, polyuria,
muscle weakness, Cl/P ratio >33:1, ECG: shortened QT interval.
Rx:
i) For hypercalcemic crisis: vigorous IV fluids, fluids, fluids--Add Pamindronate and---
Add calcitonin----Add furosemide
ii) If sarcoidosis: Steroids

iii) If due to malignancy (M.M, breast) = Bisphosphonates (Zolendronic acid) v.v.imp mcq

Mtb-3.. 3-4 L OF N/S..+add furosemide+Calcitonin faster than bisphosphonate

Note
i) The most common cause of hypercalcemia /asymptomatic hypercalcemia/
hypercalcimeia in ambulatory patients = primary hyperparathyroidism (
ii) Most common cause of Symptomatic hypercalcemia = PTH-like peptides (eg. Malignancy scc lung,
breast, MM)

iii)
PTH
Vitamin-D
Increased absorption of Calcium from Increased absorption of calcium from
Distal tubule
Proximal GIT
PO4 excretion from kidney
PO4 absorption from Proximal tubule in
kidney

Primary
Hyperparathyroidism

Malignancy related
hypercalcemia

Sarcoidosis

Familial
hypercalcemic
hypocalciuria

Mild serum calcium

elevation

Severe serum calcium

elevation

Mild serum
calcium
elevation

Mild serum
calcium
elevation

May or may
not be
symptomatic

No symptoms

Causes:
Occasional hypertension

i) Cytokines = IL1 , TNF by

metastatic breast , lung
cancer
ii) PTH related peptide by Sq
cell ca . It causes body PTH
level to be suppressed
iii) Ectpic PTH production by
ovarian tumor, lung, nect
iv) Calcitriol production
causes hypercalcemia in
Hodgkin disease (

Asymptomatic

Symptomatic

They get
hypercalcemia
mostly in
summer b/c of
increased sun
exposure and
increased
vitamin D
Elevated PTH

Low PTH

Low PTH but

elevated
vitamin D

Normal or
slightly low PTH

Low urine
calcium
Treat by surgery

Indications:
i) Symptomatic

Treat symptomatic
hypercalcemia by fluid fluid
fluid-
Furosamide.Calcitonin-

Treat with
steroids

Treat underlying cause

ii) Asymptomatic with:

a) Serum calcicum atleast
1mg/dl above upper limit
of normal
b) Urinary calcium
>400mg/24 hours
c) age <50 years
d) DEXA showing bone
mineral density <2.5 at any
site
e) GFR <60

Milk alkali syndrome : Hypercalcemia, Metabolic alkalosis, Renal insufficiency

Develops if calcium intake >2.5g/day (

Immobilization leads to accelerated bone resorption leading to hypercalcemia
with decreased PTH levels. This effect of immobilization is pronounced in
young healthy patients and the patients with Pagets disease.

6) Hypoglycemia in diabetic patients :

i) Insulin overdose: wrong dose, recent lifestyle modification eg exercise
ii) New onset Renal failure

7) Hypoglycemia in non-diabetic patients:

i) Prolonged fasting
ii) Insulinoma
iii) Exogenous insulin administration (Factitious)
iv) Exogenous Sulfonylurea use
v) Adrenal, Liver failure

Insulin
C-peptide
Pro-insulin

Anti-insulin
Ab
Urine
sulfonylurea

In diabetic

Factitous

Insulinoma

(>5 or >20% of total

immunoreactive
insulin)

Sulfonylurea
use

(<20%)
or normal

Yes
Yes

Polonged
fasting

8) A patient with features suggestive of hyperthyroidism

Graves
Enlargment of
gland
Pain
Eye and skin
signs
RAIU

Toxic MNG

Factitious

Diffuse

Subacute
thyroiditis
Diffuse

Nodular

No

No
Yes

Yes
No

NO
No

No
NO

Diffusely
increased
TSI antibodies Yes
Other

Treatment

i) Make
patient
euthyroid
(Bb,
antithyroid

Decreased

Focally
increased
No
No
History of viral i) Cardiac
illness and if
signs more
biopsy done it pronounced
shows
ii) History of
Multinucleated goiter in past
foreign body
giant cells
Just supportive Surgery
and give NSAID

Decreased
NO
History
findings

ii) RAI
ablation
(definite
treatment)
Note:
i) RAI ablation is contraindicated in Pregnancy and severe ophthalmopathy
ii) Antithyroid drugs are used mainly during Pregnancy and in preparation of
Surgery or RAI ablation to make patient euthryoid

iii) For thyroid storm: Propranolol, Antithyroid, Iopanoic acid and Ipodate,
Steroids.

10) Congenital Adrenal Hyperplasias

21 hydroxylase
11 hydroxylase
17 hydroxylase

Blood pressure

Androgens

Measure urinary 17 OH steroids (elevated esp in 21 hydroxylase deficiency)

ELECTROLYTES AND FLUID

1) Hypernatremia may be Hypovolemic, Euvolemic and Hypervolemic.
Hypovolemic
Euvolemic
Hypervolemic
(Fluid loss but greater
(Just sodium retention)
water loss as compared
(Fluid retention with
to sodium)
greater sodium
retention)
Pani bohat kam so
Sodium retention
sodium zyada eg: (less Eg: Diabetes insipidus
intake of water,
increased loss of water,
watery diarrhea)
Rx:
Rx: 5% dextrose in
5% dextrose in water
i) Isotonic 0.9% Saline
water
which acts gradually to
correct the hyper-

osmolarity. Once
volume deficit is
restored switch to
0.45% Normal saline.
ii) For mild: 5%
dextrose in 0.45%
normal saline
212`
Note: Do not correct
sodium >1 mEq/L/h b.c
may result in cerebral
edema
2) Metabolic alkalosis is characterized by an alkaline pH and primary increase in
serum HCO3 level >24 mEq/L.
Chloride sensitive/ Saline
sensitive/Hypochloremic
Urinary chloride <20mEq/day
Causes: (ECF volume contraction)
Volume contraction causes
Aldosterone which causes HCO3
retention, H+ and K+ excretion and
Sodium retention.. Urinary chloride
remains low b/c Sodium is kept in
body as NaCl.
i) Excessive vomiting/ GOO/
surreptitious vomiting
ii) Thiazide diuretics
iii) Loop diuretics

Chloride resistant/Saline
resistant/Hyperchloremic BUT
HyPOKALEMIC
Urinary chloride >20mEq/day
Causes: (ECF volume expansion)
i) Conns syndrome (Inc Ald/renin ratio
is most specific)
ii) Barter syndrome
iii) Gitelman syndrome
iv) Excessive black lacorine ingestion
(Just like Conn but low renin and low
aldo)
v)) Thiazide diuretics (uw says)
vi) Loop diuretics
In barter:
Volume depletion Increased
renin.. Increased aldosterone.
Increased sodium/Dec potassium

Chloride is kept in body

Corrected by giving Normal saline

Chloride is lost in urine

Not corrected by giving normal saline

A normotensive patient wit HYPOKALEMIC METABOLIC ALKALOSIS:

i) Diuretic use
ii) Surreptitious vomiting
iii) Barter
iv) Gitelman

DERMATOLOGY
1) Vascular tumors
Hemangiomas

Cherry hemangioma
(most common benign
vascular tumors in adults)

L/M: proliferation of
capillaries and post
capillary venules in
papillary dermis

Small, red, cutaneous papules

, bright red , dome shaped, in
aging adults.
They do not regress
spontaneously and typically
increase in number with age

Cavernous hemangioma
(May appear on skin, mucosa,
deep tissues and viscera)
These are the most common
benign tumor of liver and
spleen) Rapidly enlarge and
then regress by 5-8 years
May involve larynx and may
cause laryngeal obstruction
If large can cause high output
cardiac failure due to
increased vascularity

They are only

superficial, not deep

Cavernous
hemangioma of brain
and Viscera are
associated with Von
Hippel Lindau disease
(A.D)
Soft blue compressible masses
upto few centimeters.
May squaster the platelets
and RBC and decrease their
number

VHL: associated with

pheochromocytoma
and bilateral RCC

1st line therapy = Steroids

If fail= Interferon

Strawberry hemangioma
(appear during first weeks of
life, initially grow rapidly and
regress by 5-8 years)

They regress
spontaneously but if
become ulcerated,
GIVE PROPRANOLOL
They are bright red,
compressible with sharpely
demarcation when near
epidermis, and more
violaceous when deeper,

Spider angioma

Bright red central arteriole

surrounder by several
outwardly radiating vessels.

Angiomyolipoma
Angiosarcoma

Kidney hamartoma consisting

of Blood vessels, muscle and
mature adipose tissue
L

Bacillary angiomatosis
(Exophytic skin lessions with a
collater of scale which are
pedunculated) Lesions are
prone to hemorrhage
Benign capillary proliferation
involving skin and visceral
organs
Prone to hemorrhage

Kaposi sarcoma
(Leg, face, oral cavity,
genitalia)
Bacillary
Red
Involves
viscera ESP
liver
Capillary
proliferation

K.s
Color change
Involves
viscra (GIT
LUNGS)
Mesenchymal
proliferation

Malignant tumor arising from

proliferation of endothelial or
primitive mesenchymal cells
Color change from red brown
to violet/ purpulish

They occur due to the

dilation of central
arteriole and its
superficial capillary
network and are
estrogen dependant
Found in Cirrhosis
patients and
pregnancy
Assosication with
tuberous sclerosis
Liver angiosarcoma
associated with
exposure to PVC,
Arsenic, Thorium
oxide
Found in AIDS
patients caused by
gram negative
bacillus: BARTONELLA
HENSALE.= also fever,
wt loss, malaise, abd
pain, and liver mass.
Rx: Doxy, Azithro,
(dont confuse it with
Kaposi sarcoma)
Found in AIDS
patients WHICH IS
ONLY ACQUIRED
THROUGH SEXUAL
CONTACTcaused by
HHV-8

Pyogenic granuloma

Post traumatic or
associated with
pregnancy (related to
estrogen)
Vascular red pedunculated,
ulcerates and bleeds.

Heredrity hemorrhagic
telengectsia (osler weber
rendau) A.D
Sturge Weber syndrome
SKULL X-RAY TAKEN AFTER 2
YEARS SHOW GYRIFORM
INTRACRANIAL
CALCIFICATIONS WHICH
RESEMBLE A TRAMLINE
Nevus is due to Cavernous
hemangioma

Nevus flammeus (birthmark/

port-wine stain) on face in the
distribution of ophthalmic
branch of trigeminal.do NOT
BLANCH ON PRESSURE
Mx: If facial nevus found on
birth Measure IOP Do
skull x-ray. Do CT
i) Skull x-ray: occipital-parietal
calcification
ii) CT: to show extant and
unilateral cortical atrophy and
hydrocephalus ex vacuo
Rx:
i) Seizure management
ii) Hemispherectomy or
lobectomy in 1st year.
iii) Regular IOP checking
iv) Pulsed laser for nevus

Lichen planus
(Dx with Deep Punch biopsy)

Pruritic, planar, purpule,

polygonal papules n plaques
on flexor surfaces esp WRIST,
Wickam striae (white lacy),
Mucous membrane have fine

Some cases may

show ipsilateral
malformation of pia
mater vessels
overlying occipital
and parietal lobes.
i) Facial nevus in
distribution of
trigeminal
ii) Glaucoma in
ipsilateral eye
iii) Seizure (most
common
presentation): focal
tonic clonic,
contralateral to
nevus, becomes
refractory and
slowely develops
hemiparesis and
mental retardation
iv) Can develop
hydrocephalus
Associated with HCV,
autoimmune
disorders and color
developer handlers

lacy white pinhead sized

papules

Note:
i) Port wine stain(nevus flammues/birthmark): it is vascular malformation and
permanent defect which is unilateral and on head and neck. Rule out sturge
weber syndrome Rx: Pulsed Laser
ii)

2) Hypersensitivity reactions involving skin

Urticaria
Causes:
Acute: Drugs, insect,
food (peanut), emotions,
latex.
Non-igE mediated but
still mast cell activation =
Radiocontrast, NSAID,
opiate, EBV,
hep b (it is just like
serum sickness as type 3
hstn)
Chronic: Pressure on
skin, cold, vibration,
autoimmune or
associated with
angioedema

Type-I hypersensitivity ;
Mast cells release
histaminegiving rise
to a Localized
anaphylaxis

Edematous wheals (hives) that

are fleeting in nature i.e: they
disappear within hours and
reappear at another location..
They blanch with pressure.
Lesion get worse with
scratching. & they cause intense
pruritis or stinging,
Dermatographism(develop in
areas of mechanical pressure on
skin)
Biopsy: * MCQ *
INTRADERMAL EDEMA WITH
LEUKOCYTE INFILTRATION

Acute = <6 weeks

Chronic=>6 weeks
Rx:
Acute:
i) Older antihistamines
ii) If systemic signs: add
steroids
Chronic:
i) New antihistamines
ii) Desensitization (if
trigger cant avoided)
Note: Beta blocker must
be stopped prior to
desensitization b/c they
inhibit the effect of
epinephrine that may be
used if there is
anaphylaxis during
desensitization
(v.imp mcq)
Note:

ANGIOEDEMA
(occurs in deep skin than
urticarial i.e in
subcutaneous tissue)
Causes:
i) Heredrity: Deficiency of
c-1 esterase inhibitor
ii) Acquired: minor
trauma, ACE inhibitors
best initial test:
Decreased C2 and C4

Eyes, lids, lips, tongue, genitalia,

hand or feet are affected giving
non-pitting edema. It is more
burning than pruritic.
Severe angioedema may lead to
life threatning airway
obstruction
Tracheostomy ki zarurat bi par
skti ha (

Labs will show ed C2

and C3 in c-1 esterase
deficiency
C2b, Bradykinin
Normal C1q

IN complement pathway
Edema producing factors: C2b,
bradykinin
Chemotactic: C5a
Opsonization: c3b

Note: c1q is low in

familial SLE

Pehly Subcutaneous
epinephrine deni ha agr phir bi
bnda ki oxygenation thek nai
horhe to phir ETT

Angioedema can be easily

diagnosed from the rapid
onset of symptoms which
include non-inflammatory
edema of face, limbs,
genitalia; laryngeal edema;
and edema of the bowels
resulting in colicky pain.
Laryngeal edema can result

Note about HEREDRITY ANGIOEDEMA...

jo sedhy sedhy 1, 2, 3, 4 hain wo
decreases = C1 estrase inhibitor, c2, c3,
c4 decreased
but agr kisi bi C1,2,3 etc k sath koi word
"a" ya "b" lga do to wo increase hoga =
Increased C2b, C3a, C5a... (but C1q
normal hoga)

i) If H1 alone dont work

= add H2 as well
ii) For chronic refractory
angio/urticarial = IvIg or
plasmapheresis
Rx:
For acute: give FFP
Treat just like
Anaphylaxis: look
airway and if
obstruction.. secure
airway and
i) Subcutaneous
epinephrine (v.v.v.imp
mcq)
ii) Corticosteroids
iii) Antihistamines
(diphenhydramine)
.IF no response
Shift patient to ICU and
secure airway
Note: If signs of
respiratory failure like
cyanosis and obtudation
are there = do ETT
before giving
epinephrine
For heredrity
angioedema
i) Ecallantide (d.o.c)
it is inhibitor of kallikrein
hence stops bradykinin
production

in life threatening airway

compromise. Both hereditary
and acquired forms of C1
inhibitor deficiency exist with
similar clinical manifestations.
The deficiency leads to
elevated levels of edemaproducing factors C2b and
bradykinin. Patients with
hereditary angioedema
usually present in late
childhood.
Usually, episodes of
angioedema follow
infection, dental
procedures, or trauma.

BULLOUS
PEMPHIGOID
PEMPHIGUS
VULGARIS
CICATRICIAL
PEMPHIGOID
CONTACT
DERMATITIS

ii) Androgens (Danazol/

Stanazol) they raise C1
estrase inhibitor levels

Type 2 hypersensitivity involving

IgG antibodies against basement
membrane glycoproteins BP-320
and EP-180. And biopsy shows
IgG and C3 deposit in linear
pattern in dermal-epidermal
junction (v.v.v.imp mcq)
Type 2 hypersensitivity involving
IgG antibodies against
Desmosomes in intra-epidermal
junctions
As they are located above the
basal layer , the basal layer gives
Tombstone appearance
IgG deposits in linear pattern at
dermal-epidermal junction (dif
from B.P = cicatricial does not
involve skin)
Type-4 hypersensitivity.
i) Allergic contact dermatitis:
Poison ivy, Nickel
Poison sumac: from firewood (
ii) Irritant contact dermatitis: eg
laundary detergent
iii) Contact photodermatitis: UV
rays react with drugs having
photosensitizing effect eg:

Tense bullae, subepidrmal blisters in

flexural areas in old
patients >60 years.
Intense pruritis
Flaccid blisters intraepidermal on skin and
oral mucosa inpatients
<60 years
No pruritis
Mouth, oropharynx,
conjunctiva, nares,
genitalia
Linear streaked vesicles
esp if caused by poison
ivy

ATOPIC
DERMATITIS
Mechanism:
Decreased skin barrier due
to improper synthesis of
epidermal cornified cell
envelope & immune
system hyperactivity

Tetracycline Erythema, edema

and vesicles
(
iv) Diaper dermatitis
Type 1 hypersensitivity
Children: Dry skin and eczema
on cheeks and extensor
surfaces, face, scalp but diaper
area is spared.
Adults: Dry skin and eczema on
hands, eyelids, flexor surfaces
Most common symptom is
PRURITIS. In infants the lesions
are symmetrical (

Start as erosions with

serous exudates,
intensely itchy papules
or plaques over
erythematous skin
Rx:
i) Skin care:
Moisturizers, avoid bath
and soap, use cotton,
use emollients
ii) Drugs:
Topical steroids, Topical
tacro and pimercolimus,
Antihistamines (for
severe DOXIPENE),

Exfoliative
dermatitis
(Erythroderma)

PRIOR psoriasis, atopic

dermatitis, Sezary syndrome
(mycosis fungoides)

Dermatitis
herpetiformis

is an uncommon disorder in
which groups of intensely itchy
blisters appear on elbows
shoulders, buttocks and knees.
There may be an associated gluten enteropathy Skin
biopsy characteristically shows subepidermal
microabscesses or blisters and
immunofluorescence shows
granular IgA deposits in dermal
papillae .Patients with this
disorder have a high association with HLA B8 (85-90%) and
DRw3. Although the dis-

Itchy (also bullous

pemphigoid is also itchy)

ease is well controlled with

dapsone and a gluten-free diet,
treatment may be long term as
the condition persists for many
years, and there is some
evidence to suggest a risk of
small
bowel lymphoma, as in coeliac
disease.

ACE INHIBITORS AND ANGIOEDEMA:

3) A patient with Pale, velvety pink/whitish hypopigmented macules that do not
tan and do not appear scaly (but normal skin tan); sometimes hyperpigmented as
well, Lesions are not scaly but scale on scraping/ rubbing and arranged in raindrop
pattern/ confluent pattern on chest , back sometimes lesions more apparent
after sun-exposure = TINEA VERSICOLOR/ PYTRIASIS VERSICOLOR Caused by
M.furfur which is a saprophytic lipid dependant and dimorphic yeast Best initial
test: KOH preparation = Spagetti and meatball appearanceRx: topically with
SELENIUM SULFIDE and ketoconazole shampoo., oral ketoconazole (best). Uw
Hot/Humid condition me M.furfur converts into hyphae form and causes lesions
Hyperpigmented type
Enlargment of melanosomes

Hypopigmented type
Decrease in melanin due to tyrosinase
inhibition by fungus derived acids
(Dicarboxylic acid)

4) History of normal skin at birth with gradual progression to dry scaly, rough skin
with horny plates over the extensor surface of the limbs = ICHTHYOSIS this
condition worsens in the winter season b/c of increased dryness and is reffered as
Lizard skin
5) A patient of Atopic dermatitis with umbilicated vesicles over erythematous skin
on both cheeks = ECZEMA HERPETICUM it is a form of primary herpes simplex
in atopic dermatitis patients. It is superimposed on healing atopic dermatitis after
exposure to herpes simplex associated with fever and adenopathy. Rx:
acyclovir (

6) Scaly, yellowish, Greasy rash involving Scalp, Eyebrows, Nasolabial folds =

SEBORRHIC DERMATITIS. P/e: Waxy scales with underlying erythema on
face, presternal area, interscapular area, umbilicus and body folds.. Associated
with HIV and Parkinson.. in children called CRADLE CAP.

7) A patient with Firm, Flesh-colored, Dome / Bowl shaped, Umbilicated lesions

on trunk, limbs and anogenital regions which are non-pruritic, white material can
be extruded when they are squeezed = MOLLUSCUM CONTAGIOSUM (poxvirus) Depression contains viral particles called molluscum
bodies..More common in Immunocompromised patients esp AIDS <100 CD4
count also, corticosteroid use and chemotherapy patients. Can be transmitted

sexually and by self-inoculation .. Rx: Liquid nitrogen curettage , use ritonavir ,

cidofovir in AIDS (

8) A newborn with Pearly white papules on face, gingiva, midline of palate =

MILIA.. These are actually superficial epidermal inclusion cysts that contain
laminated keratin material..Rx: Exfoliate spontaneously or can be unroofed with
fine needle.. If milia are in mouth, they are called EPSTEINS PEARLS.

Miliaria Crystallina
Pinpoint clear vesicles on skin
Retention of swet in eccrine sweat
glands

Miliaria Rubra
Erythematous papulovesicles
imparting prickly heat sensation
Retention of sweat

Miliaria are associated with warm humid condition and respond to cooling like
prickly heat powder
9) Superficial fungul infections (Dermatophytes)
i) Tricophyton

ii) Microsporum

iii) Epidermophyton

Microsporium gives bright blue-green fluorescence on woodlamp whereas

tricophyton does not give (remember M=W)
Best initial test: KOH preparation
Most accurate test: Fungul culture
Tinea Capitis
(
i) More common in
blacks

Scalp
Blacks: Tricophyton
tonsurans (most
common), negative
woodlamp

Oral Terbinafine or
Griseofulvin/
Fluconazole/ Itraconazole
for 1 month after culture
negative (v.imp mcq)

ii) Black dot ringworm.

(area of alopecia has
black dots indicating hair
has broken off close to
hair follicle)v.imp (not
true alopecia areata)

White:
M.canis/audouinii,
positive woodlamp

Topical drugs are not

effective

Oral GRISEOFULVIN is
Circular ring shaped
preffered and if it is
patches of hair loss
resistant =use ORAL
(alopecia areata).This TERBINAFINE.
iii)Keroin is a severe
alopecia develops into
(remember: SAR
inflammatory response
Keroin (Large, boggy,
KHANA means sar k lea
and has elevated, boggy, tender, erythematous
oral)
granulomatous mass that swelling with viscous
does not contain pus exudate associated with Note: Only
so never do INCISION
cervical and occipital
Onychomycosis and tinea
AND DRAINAGE but treat adenopathy
capitis are treated orally,
with oral steroids
other topical infections
treated topical drugs.

Tinea corporis
Note: Pytriasis rosea are
also oval shaped and
scaly but there is no
central clearance, instead
center has pink,
crinckled, cigerrate paper
like appearance and

Ringworm, ANNULAR
with and elevated red
scaly outer border and
central clearing
Annular rash with
central clearance:
i) Tinea corporis
ii) Lyme disease

Onychomycosis:
treatment of choice is
oral Terbinafine and
Itraoconazole. 6 wks for
finger nail infx and 12
wks for toenail infx. New
TOPICAL antifungal for
onychomycosis is
Ciclopirox use for mild to
moderate infx, although
safe but minimal efficacy.
All treated by topical
antifungals (Miconazole,
Clotrimazole,
ketoconazole, nystatin,
ciclopirox) for 4-8
weeks
2% terbinafine

initial larger lesion is

called Herald patch

Pytriasis rosea is associated with

HHV-7

Tinea pedis
Tinea cruris

Athelete foot
Jock itch

10) An fair skin old patient with Coin like macular to raised verrocuoid,
cerebriform,, greasy, dark lesion giving Stuck on appearance = SEBORRHEIC
KERATOSIS. Mostly found on face, shoulder, chest and back.. Rx: remove
only for cosmetic purpose with liquid nitrogen or curettage Leser-Trelat
sign = Rapid increase in number of seborrhic keratosis which is a phenotype
marker for gastric adenocarcinoma.
Seborrhic keratosis is also known as barnacles of old age. They can occur
anywhere except palms and soles
11) Baldness
Cicatricial alopecia (due to
scarring)

Androgenic baldness
Alopecia areata

i) Due to fungal, bacterial viral or systemic

disesase (SLE, CREST), ionizing radiation
ii) It is irrerversible

Use 5% minoxidil topical or finestradie

i) patches of hairloss
ii) thin exclamation marks hairs are seen
*Inject steroids and do VDRL test.* iii) Can become alopecia totalis
iv) Associated with Hashimoto, pernicious,
MCQ Q-BOOK. Page:42
Addison, vitiligo, also can be found in
SYPHILIS (v.imp mcq)
v) Treat topical injection/ intralesional
corticosteroids (v.imp mcq)

Telogen effluvium
(one study showed that the main
cause of telogen effluvium is IRON
DEFICENCY)
CMDT-2012-PAGE: 158

Diffuse hair loss after pregnancy, febrile

illness, severe medical illness, or
operations, cytotoxic drugs, Iron
deficiency, hypo/hyperthyroidism, SLE,
ocp, vit-a derivatives
Hair lost after combing or shampooing
o/E: large number of hairs with white bulb
coming out on gentle tugging

Trichotillomania
13) Middle aged fair skin person with abnormal flushing of face in response to
various substances eg( alcohol)..also found pustules, papules, Talengectasias..
ROSACEA....... treat with topical metronidazole also systemic tetracycline or
isotretinoin
i)Nose becomes thick and greasy due to sabecous gland hyperplasia=
rhinophyma
ii) Caused by mite=Demodex follicolurim
iii)

Ocular involvement may happen in rosacea.

Episodic flushing for 2030 sec with diarrhea,

telengectasias may be
there
Carcinoid

Flushing after hot and

alchol intake and last
longer with papules and
pustules, telengectasias
Acne Rosacea

Papules and pustules

with comedomes and no
Telengectasias
Acne vulgaris

A 54 years old male from Pakistan presents to you with complaints of generalized
malaise, fever and cough. He claims that he has had intermittent hemoptysis for
the past 6 months. He denies smoking but remembers a history of tuberculosis in
past treat with ATT. Examination is unremarkable and his chest X-RAY is shown. On
changing position you notice that the part of the lesion seen of x-ray also moves.

Which of the following is the most likely diagnosis?

a) Lung abscess
b) Pulmonary embolism
c) Aspergilloma
d) Allergic bronchopulmonary aspergillosis
e) Histoplasmosis
f) Bronchiectasis
g) Coccidiomycosis

PSYCHIATRY HIGH YIELD

1) A patient with s/s of acute mania and agitated 1st step in management..Give
Resperidone.. Then give Lithium as a mood stabilizer.. but remember one thing to monitor
Lithium becoz it has got so many adverse effects and it has narrow therapeutic index.
Side effects of Lithium: Therapeutic level (0.8 -1.2) if >1.5= toxicity
1) Acute: GIT: Nausea, vomiting, diarrhea
2) Chronic: CNS: Ataxia, confusion, tremors, exaggerated DTR
3) Others: Weight gain, Nephrotoxicity (>2 level), Hypothyroidism, D.I, Acne, teratogenic
What predisposes to lithium toxicity?
i)
Overdose
ii)
Drug interactions (esp the drugs that affect kidney., the drugs which affect
GFR and electrolyte disturbances most likely Thiazide)
iii)
Old age
iv)
Dehydration/ Vol depletion

1) VARACILLA ZOSTER VACCINE IS ALTHOUGH GIVEN IN CHILDHOOD AT 2 DOSES

AFTER 12 MONTHS BUT IT SHOULD ALSO BE GIVEN TO EVERY PERSON >60 YEARS OF
AGE TO PREVENT FROM DEVELOPING SHINGLES AND PHN. EVEN IF THAT AGED
PERSON HAS GOT SHINGLES FIRST TIME, HE MUST BE GIVEN VACCINE WHEN HE IS
>60 YRS.
2) VARACILLA ZOSTER IMMUNGLOBULIN :
1) GIVE TO SUSCEPTIBLE CHILDREN AND HOUSEHOLD CONTACTS
2) SUSCEPTIBLE PREGNANT WOMAN
3) NEWBORN (IF HIS MOTHER HAD CHICKENPOX WITHIN 5 DAYS BEFORE TO 48
HOURS AFTER DELIVERY)

3) If an immunocompetent patient gets varicella zoster ... he/she not needs to be

isolated because it is unlikely to be transmitted to other ppl until he covers his
lesions........... but if immunocompromised pt develops varacilla or any person
develops dissminiated varacilla, he should pe kept in complete isolation until all
lesions are dry and crusted............... but remember one thing, the primary
varacilla zoter (chickenpox) is highly contagious and can even spread via droplet
infection

LIVE LIKE MUHAMMAD (S.A.W.W)

& ALI (A.S)
DIE LIKE HUSSAIN (A.S)
STAY BLESSED
FROM: DR. SHAHERYAR ALI JAFRI
(AIMC)