Practice Questions

Question 1

Leykocyte adhesion def is caused by what cd molecule

Answer 1

CD18
Aka intergin beta-2
Without it there is no adhesion dependent migration from vessel to outside
Hence no pus recurrent inf —-gm neg staph aureus and fungus
Delayed cord separation

Question 2

Name the steps of neutrophil response in inflammation

Answer 2

Margination 
Rolling
Adhesion
Extravasation 
Chemotaxis

Question 3

Name the steps of neutrophil response in inflammation with their mediators

Answer 3

Margination—-nitrous oxide and vasoactive substances

Rolling—-P & E Selectins and glycoproteins

Adhesion- CD18 intergin beta 2 ICAM PROTEINS

EXTRAVASATION- integrins and pseudopodia

Chemotaxis— interleukin 8, C5a, LtB4 and formly methionated proteins

Question 4

cherry red spot in macula is a sign of

Answer 4

central retinal artery occlusion.
There is diffuse retinal ischemia and macula is spared.
since macula recieves its blood supply from choroid by long and short posterior ciliary arteries

Question 5

JAK 2 gene mutations are associated with

Answer 5

polycythemia vera
primary myelofibrosis (increased megakaryocytes stimulate collagen release from other cells and cause myelofibrosis)
essential thyombocythemia

Question 6

PRCA is seen with

Answer 6

thymic mass lesions
lymphocytic leukemia

due to autoimmune destruction by Cytotoxic T cells or IgG autoantibodies against RBC precursors only

Question 7

herpes like vesicular excoriating lesions in extensor surfaces elbow and knees
in a patient with voluminous stools indicate

Answer 7

dermatitis herpatiformis in a patient with celiac disease

Question 8

renal affection in patients with PNH

Answer 8

Hemolysis — hemosiderosis in kidney — proximal tubular function affected
Pts have vascular thrombosis at various sites.
In kidney too can lead to microvascular thrombosis leading to cortical infarcts and interstitial scarring.
ultimately — CRF.

Question 9

proximal girdle muscle weakness with skin changes should prompt what diagnosis

Answer 9

muscle + skin = dermatomyositis – autoimmune disorder

Question 10

causes of dermatomyositis

Answer 10

isolated
secondary autoimmune as paraneoplastic syndrome
malignancy— adeno ca of lung pancreas and ovary

Question 11

skin manifestations of chronic HCV

Answer 11

1. Prophyria cutanea tarda— skin blistering in sun exposed area
2. Mixed cryoglobulinemic vasculitis — non blanching palpable purpura.

Question 12

acanthosis nigrans is associated with

Answer 12

insulin resistance of anytype - DM, cortisol excess cushings, obesity
Visceral malignancy – stomach adenoca

Question 13

myositis with normal CK levels

that is no myocyte damage is occuring

Answer 13

1. GLUCOCORTICOID induced myositis (cushings- 24hr urinary cortisol is elevated, catabolic effect on muscle) Lower limbs affects. Condition is painless.
2. POLYMYALGIA RHEUMATICA- Painfull stiffness of proximal upper limb and lower limb muscles.
   Pain and weakness more on exercise or work and in morning.

Question 14

myositis with elevated CK levels

Significamnt myocyte damage is occuring

Answer 14

1. Statin induced myositis (history of statin intake)
2. hypothyroid induced (delayed tendon reflexes and myoedema)
3. Inflammatory myositis – DM and PM has rash and inflammatory arthritis.
4. Inherited muscular dystrophies.

Question 15

slow relaxation of ankle jerks

Answer 15

hypothyroidism

Question 16

elevated pronormboblasts with intranuclear inclusions is a characteristic sign of

Answer 16

problem with maturation of erythyroid precursors

esp transient aplasia or parvovirus B19 infection

Question 17

DIC is excessive activation of which coagulation pathway

Answer 17

extrinsic pathway (7a, 10a, thrombin, fibrin, crosslinked clot)
tissue factor wala.
like heat exhaustion causes tissue necrosis and hence DIC
or fetal death causes tissue factor release in blood and then DIC

Question 18

what are changes of DIC In blood

Answer 18

thrombin and clots increase
Fibrinolysis increase to lyse those clots
Plasmin increase to lyse those clots
Fibrin degradation products produced from lysing of those clots increase– ie D dimer increase
Anticoagulants protein C and S and antithrombin thus gets consumed and depleted.

Question 19

DIC effect of blood coagulation studies

Answer 19

Platelets consumed— Platelet count reduced
Coagulation factors consumed- PT and APTT increased
bleeding time is no longer done.

Question 20

lysozymes and defensins are secreted by which intestinal epithelial cell

Answer 20

paneth cells at the base of intestinal crypt.

they are first line defense for mucosal infection

Question 21

Shiga like toxin is secreted by which bacteria, infects which organ and damages which organ.
Remember all three answers are unique

Answer 21

Shiga like toxin is produced by GIT infection from E Coli O157 :H7
Toxin travels in blood and damages endothelial cells of kidney leading to uremia ARF.

Question 22

Shigella infects what cells

Answer 22

gains access through Microfold cells (M cells ) in the peyers patch. Entry is through endocytosis.
multiplies, lyses the endosome and spreads laterally to other adjacent cells. Denudation, haemorrhagic diarrhoea ulceration.

Question 23

RBC lacks mitochondria. so TCA krebs and ETC does not happen. How many ATP are generated for one molecule of glucose

Answer 23

4 generated two used- net is 2 ATP.
ATP producing steps are 1-3 BPG —> 3PG gives 2 ATP
and pyruvate kinase step PEP —–> pyruvate gives 2 ATP
Hence in pyruvate kinase deficiency RBC losses all ATP stops membrane function and rigid and undergoes extravascular hemolysis in splenic red pulp.

Question 24

which patient would show pyruvate kinase deficiency

Answer 24

newborns – hemolytic anemia in newborn.
Have increased 23 BPG, HB releases Oxygen easily.
kids have anemia and splenomegaly.

Question 25

Lab findings in von willebrands deficiency

Answer 25

Platelet count and function is normal.
Bleeding time is prolonged.
vWf carries and protects factor 8 which is starting point of intrinsic pathway. Hence APTT is prolonged because factor 8 is less or degraded more.
PT marker of extrinsic factor 7 and combined pathway is normal.

Question 26

what type of bleeding occurs in uremia

Answer 26

GI bleeding. Uremic platelets are dysfunctional because they cannot produce enough thromboxane A2.

Question 27

heparin induced thrombocytopenia and thrombosis is due to

Answer 27

heparin binding to platelet factor 4 and forming a complex on surface of platelet
An antibody response to this complex mounts the prothrombotic disease–positive feed back loop
called heparin induced thrombocytopenia

Question 28

treatment of heparin induced thrombocytopenia and thrombosis

Answer 28

discontinue heparin,
dont give warfarin or platelet transfusion.. worsens
Give DTIs= direct thrombin inhibitors because thrombosis needs to be stopped.
DTIs approved are =arga-tro-ban and bivalirudins.
Indirect TI used are – fondaparinux and danaparuid.

Question 29

causes of IgE independent mast cell degranulations

Answer 29

Drugs IV like

Opiates, Radiology contrast dyes and vancomycin

Question 30

What is the pathogenesis of IgE independent mast cell degranulation

Answer 30

Activation of enzymes protein kinase A and PI3 kinase by drugs like opiates, radiocontrast dyes and vancomycin.

Question 31

leflunomide inhibits which enzyme

It is used to treat

Answer 31

DHODH– dihydro-orotate dehydrogenase (pyrimidine synthesis- T cell proliferation)

Used in rheumatoid and psoriartic arthritis

Question 32

absent cremasteric reflex

Answer 32

lapro surgery injury to genitofemoral nerve.

L1-L2

Question 33

Calmodulin and myosin light chain kinase are associated with what type of muscle contraction

Answer 33

Smooth muscle contraction.

Question 34

Effect of epinephrine action on skelatal muscles

Answer 34

Acts on B2 adrenergic receptors— increases skeletal muscle blood flow (flight needs to run)
Glycogenolyiss (energy for running in flight mode)
Lipolysis (energy for running in flight mode)

HENCE BLOOD FLOW, GLYCOGENOLYSIS AND LIPOLYSIS