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MOD > CIS things I missed > Flashcards

CIS things I missed Flashcards

1
Q

What does an apoptotic body look like on H and E?

what is this a part of and what is the major hallmark?

A

brightly eosinophilic cytoplasm and condensed nucleus

chromatin condenations –> apoptosis

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2
Q

What are the 4 reasons for apoptosis?

A

DNA damage

accumulation of misfiled proteins

cell death in infection

pathologic atrophy in parenchymal organs after duct obstruction

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3
Q

what directly activates ignitor caspases?

A

FADD

Cytochrome C

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4
Q

Another name for acid maltase?

what disease?

A

Lysosomal Glucosidase

Pompe

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5
Q

what do you see on the CXR for pulmonary edema

A

white streaking

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6
Q

why do women with testicular feminization syndrome need testicular surveillance?

A

they have normal testosterone and the testes have just not descended.. so they’re at a greater risk for cancer.

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7
Q

What cytokines are found in acute inflammation?

what about chronic inflammation?

A

TNF, IL1, IL6, chemokines, IL-17

IL-17, IFN-gamma, IL-12

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8
Q

What can help you figure out endocarditis?

what’s used to confirm DVTs?

A

stethoscope

Doppler ultrasound

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9
Q

What increases the production of IFN-gamma and what produces it?

A

IL-12, dendritic cells and macrophages

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10
Q

What do both 13 and 18 have that 21 does not? (2 things)

A

Rocker bottom feet

RENAL MALFORMATIONS

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11
Q

Trisomy 21, what do they have an increased risk of having before the age of 20?

A

leukemia

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12
Q

Increased levels of homocysteine increase the likelihood of what?

A

thrombus

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13
Q

what makes it worse if someone has heparin induced thrombocytopenia?

A

more platelets, more heparin.

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14
Q

What is the most important cause of primary amenorrhea?

A

Turner syndrome

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15
Q

Pyloric Stenosis?

who is it more common in

what kind of disease process is it?

A

the pyloric sphincter is too thick so the kid has projectile vomiting

it’s 3-5x more common in males

complex multifactorial pattern

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16
Q

in the question it says “elevated white count, high temp” what kind of inflammation are we looking at?

A

Acute

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17
Q

What cytokines do T lymphocytes create and what is their role?

A

TNF –> stimulates expression of stuff, systemic inflammation

IL-17 –> recruitment of neutrophils and monocytes

IFN-gamma –> activation of macrophages

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18
Q

What 3 things cause vasodilation?

A

histamine, prostaglandins (d and e and I), bradykinin

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19
Q

main function of IL-1?

A

endothelial activation.

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20
Q

What does fat emboli look like in the brain?

A

shower emboli

meaning everywhere

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21
Q

If bleeding time is on the test, what do you do?

A

don’t pick it you idiot

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22
Q

What is the EDS types for each? what are the corresponding gene defects?

Classic

Vascular

Kyphoscoliosis

A

Classic –> 1+2, COL5A1/2

4 –> COL3A1

6 –> Lysyl hydroxylase

23
Q

Difference between Niemann Pick type A and B and Niemann Pick type C?

A

C = NPC1 –> cholesterol transport

A + B –> sphingomyelinase deficiency.

24
Q

LXA4?

A

lipoxin A4 –> inhibits neutrophil recruitment and suppresses inflammation

25
Q

What are the enzymes or protein deficiencies or genes with the following diseases:

Marfan

Duchenne

Osteogenesis imperfecta

Pompe

Tay Sachs

Hunters and Hurlers

A

Fibrillen 1

Dystrophen

Collagen

Acid Maltase

Hexosaminadase A

stuff degrading glycosaminoglycans

26
Q

What is Cachexia and what is it related to?

A

state of weight loss and anorexia

TNF –> regulates energy balance by promoting lipid and protein mobilization and by suppressing appetite.

27
Q

What are the 5 things that cause increased vascular permeability?

A

histamine, serotonin

C3A and C5A (by releasing stuff from mast cells)

Leuktroienes (C,D,E)

28
Q

All storage diseases are what genotype?

A

Autosomal recessive

29
Q

What are the three possible things that signal for macrophages to eat them?

A

thrombospondin, C1Q, phosphatidylserine.

30
Q

Why do we not use Coumadin right away for someone that is prothrombotic?

A

it inactivates C and S first, leaving someone being prothrombotic –> Coumadin induced skin necrosis –> massive thrombosis with necrosis and gangrene of limbs

31
Q

What is the theory behind cleft lip? what are these called?

A

early amnion disruption –> streeter bands

32
Q

CTL mediated apoptosis?

A

CTLs secrete perforin, and this releases serine proteases called granzymes

33
Q

What’s the difference between venous and arterial thrombus CLINICALLY for someone with an extremity clot.

A

Venous –> swollen or painful and warm

Arterial –> CYANOTIC, NO PERIPHERAL PULSE. COLD

34
Q

what disease process can present with cyclops, midline defects, two vessel umbilical cord, intestines outside of the body?

A

Trisomy 13 (patau)

35
Q

When do we do a thrombin time?

A

when you’re worried about fibrinogen

36
Q

What is the outcome for most Turner syndrome babies?

A

1/4 miscarry in the first 2 months of pregnancy

37
Q

Explain Female Pseudohermpahroditism? HOW?

what can they present with too?

A

female who looks like a “fake male” –> because her body made too much adrenal androgens in the womb –> CONGENITAL ADRENAL HYPERPLASIA

salt wasting due to the congenital adrenal hyperplasia

38
Q

What do we care about for primary hypercoaguable disorders?

what don’t we look at?

A

Protein C, S, antithrombin

short PT and PTT means nothing

39
Q

What’s to know about longevity and trisomy 18 and 13?

A

both usually die within a few weeks and months

18 dies around 18 months

40
Q

What do you want to look at for a bleeding disorder?

thrombotic disorder?

A

PT, aPTT, CBC, platelet function test

genetic testing, APCR, endogenous anticoagulant levels

41
Q

Congestion causes fluid to enter a space from what mechanism?

A

hydrostatic pressure only

42
Q

What do you give an arterial clot RIGHT AWAY? why? what disease is this seen in? what kind of clot?

A

aspirin –> prevents platelet aggregation (antagonizing platelet function)

CAD

white

43
Q

How do we know someone has an inherited disease from the question stem?

A

fam hx

adopted

normal person with onset at early age

44
Q

Lipofuscin is associated with what?

what about hemosiderin?

A

ROS mediated per oxidation of lipid membranes –> wear and tear

hemorrhage or bruising.

45
Q

What artery is most likely embolized by a red thrombus?

A

pulmonary artery

46
Q

what are the 4 lysosomal storage diseases to know?

A

Tay-Sachs
Nieman Pick
Gaucher
Mucopolysaccharidoses

47
Q

Histologically what tells you it’s leukocytosis?

A

you see band cells which are earlier forms of neutrophils

48
Q

What are some examples of cardiogenic shock?

hypovolemic shock?

septic shock?

A

MI, arrhythmia, pulmonary embolism

hemorrhage, vomiting, diarrhea

microbial infections, superantigens.

49
Q

Warburg effect?

A

increase in rate of glucose uptake and production of lactate

50
Q

What does Phlebothrombosis mean?

A

venous thrombosis.

51
Q

What are the enzymes associated with hunter and hurler?

A

Hurler –> a-1-iduronidase

Hunter –>

52
Q

What is the fundamental cause of necrotic cell death?

A

reduction in ATP levels. large groups of cells die

53
Q

What arachidonic acid metabolites cause vasoconstriction?

A

Thromboxane A2, LTC4,D,E

54
Q

What can cause a paradoxical embolism in the brain or other areas than normal?

A

a patent foramen ovale –> it causes it to go to the other side of the heart and then out systemically to wherever.

MOD (8 decks)

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