Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

Pancreatitis causes

A
  1. ERCP
  2. Drugs (eg azathioprine, sulfasalazine, furosemide, valproic acid)
  3. infections (eg mumps, coxsackie, mycoplasma pneumoniae)
  4. hypertriglyceridemia
  5. structural abnormalities of the pancreatic duct (strictures, cancer, pancreas divisum) or of the ampullary region (choledochal cyst, stenosis of sphincter of Oddi)
  6. surgery (particularly of stomach, biliary tract, and cardiac surgery)
  7. hypercalcemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Crohn’s Disease labs

A

inc urine oxalate (from intestinal malabsorption) –> calcium oxalate stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pheochromocytoma

A
  • arises from neuroendocrine/chromaffin cells in adrenal medulla
  • 25% inherited (VHL, RET, NF1)
  • inc catecholamine secretion –> headaches, tachycardia/palpitations, sweater, HTN
  • Rule of 10s: b/l, extra-adrenal (paragangliomas), malignant

dx = elevated urinary & plasma catecholamines & metanephrines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Thyroiditis

A

acute, suppurative, subacute, postpartum

  • excessive release of preformed thyroid hormone
  • symptoms continuous

exam 1 q13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Carcinoid syndrome

A

excess 5HT and its metabolite 5HIAA from metastatic mid-gut neuroendocrine tumor

sx = flushing, bronchospasm, diarrhea, HoTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Schwannoma

A

peripheral nerve tumor located at cerebellopontine angle

sx = tinnitus and unilateral hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

CN III palsy

A

unilateral ptosis and gaze palsy (“down and out” gaze)

c/b berry aneurysm or uncal herniation or microvascular ischemia (e.g. due to DM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Wernicke Syndrome triad

A

ophthalmoplegia, ataxia, confusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Wernicke Syndrome cause and pathology

A

chronic thiamine deficiency –> dec glucose utilization esp in CNS
*erythrocyte transketolase levels increased after thiamine infusion

foci of hemorrhage and necrosis in mamillary bodies and periaqueductal gray matter on autopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hemolytic anemia cause

A

decreased G6PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

vitamin B12 deficiency

A

elevated methylmalonic acid levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Erythropoietic protoporphyria (EPP)

A

increased erythrocyte protoporphyrin concentration, i.e. one of the precursors of heme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cholesterol gallstones risk factors

A
  • high TG
  • combo of fibric acid derivates and bile acid-binding resins –> inc cholesterol concentration in bile
  • etoh
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sickle cell disease

A

single amino acid substitution: glutamic acid (negatively charged) –> valine (nonpolar, neutral charge) at 6th position in beta-globin chain of Hb molecule

alteration of a region on beta-globin surface that allows hydrophobic interaction among Hb molecules –> aggregation of Hb molecules –> sickling

sickling promoted by hypoxia, inc acidity, dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hb C disease

A

glu is replaced by a basic polar (positive charge) lysine

no hydrophobic interactions among Hb molecules as in SCD, hence less severe condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Saccular (berry) aneurysms

A

most common cause of SAH (AVM = 2nd most common cause)

usually occur at Circle of Willis
*Anterior communicating artery = most common site

Associated diseases:

  • Ehlers-Danlos
  • AD polycystic kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cerebral amyloid angiopathy

A

elderly patients

  • asx
  • or sx from recurrent intracerebral hemorrhages affecting small areas = HA, focal neuro deficits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Charcot-Bouchard aneurysms

A
  • lenticulostriate vessels of basal ganglia 2/2 HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

bluish neoplasm under nail bed

A

Possible origin:

  • glomus tumor (glomangioma) - thermoregulation function; tumor of modified smooth muscle cells of glomus body whose task is to shunt blood away from skin surface in cold temperature and direct it toward skin surface in hot environments
  • subungual melanoma - pigmentation fxn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

nephritic syndrome

A

HTN, hematuria, moderate proteinuria (can see pitting edema)

  1. Post-streptococcal glomerulonephritis (happens weeks after)
  2. Anti-GBM disease
  3. Rapidly progressive glomerulonephritis
  4. IgA nephropathy
  5. Alport syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Post-streptococcal glomerulonephritis

A

Ab against strep Ag cross-react with GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Anti-GBM disease

A

Ab agains type IV collagen GBM –> C3 and IgG deposition in basement membrane

these Ab can cross-react with collagen type IV in alveolar basement membrane –> pulmonary hemorrhage –> renal failure + pulmonary hemorrhage = Goodpasture syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Rapidly progressive glomerulonephritis

A

severe immune injury (e.g. anti-GBM Ab, immune complex deposition)

glomerular crescents = proliferating parietal cells with infiltration of monocytes and macrophages seen on LM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

IgA nephropathy

A

deposition of IgA-containing complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Alport syndrome

A

defective type IV collagen in GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Goodpasture syndrome

A

anti-GBM disease patient with pulmonary hemorrhage in addition to renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Familial pulmonary arterial htn

A

inactivating mx of pro-apoptotic BMPR2 gene –> inc in endothelial and smooth muscle cell proliferation

inc arteriolar smooth muscle thickness (medial hypertrophy), intimal fibrosis, luminal narrowing

progresses to plexiform lesions = tufts of small vascular channels

sx = dyspnea, exercise intolerance in women 20-40 yo

tx = lung transplant, vasodilators (e.g. Bosentan = endothelin receptor antagonist and endothelin’s vasoconstricting action)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Paroxysmal supraventricular tachycardia (PSVT)

A

c/b re-entrant impulse traveling through slowly and rapidly conducting segment of AV node

tx = slow conduction through AV node in order to abolish re-entrant circuit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

atherosclerosis

A

endothelial cell dysfunction –> macrophage and LDL accumulation –> foam cell formation –> fatty streaks –> smooth muscle cell migration (involves PDGF and FGF) –> proliferation and extracellular matrix deposition –> fibrous plaque –> complex atheromas

*occurs in the intima of elastic and large- and medium-sized arteries

abdominal aorta > coronary artery > popliteal artery > carotid artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

RFs for aortic dissection

A

HTN
bicuspid aortic valve
cystic medial necrosis (Marfan’s syndrome)
inherited connective tissue d/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Prinzmetal’s variant (anginga)

A

2/2 coronary artery spasm and occurs at rest

see ST elevation on EKG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Coronary steal syndrome

A

vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to an area of higher perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Chronic ischemic heart disease

A

chronic ischemic myocardial damage –> progressive onset of CHF over many years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

findings 0-4 hours after MI

A

gross: none
LM: none

risk for arrhythmia, CHF exacerbation, cardiogenic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

findings 4-12 hours after MI

A

gross: occluded artery, dark mottling but pale with tetrazolium stain in area of infarct

LM:
early coagulative necrosis
edema
hemorrhage
wavy fibers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

findings 12-24 hours after MI

A

gross: occluded artery, dark mottling but pale with tetrazolium stain in area of infarct

LM:
contraction bands from reperfusion injury
release of necrotic cell content into blood
beginning of neutrophil migration

risk for arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

findings 1-3 days after MI

A

gross: hyperemia

LM:

  • extensive coagulative necrosis
  • tissue surrounding infarct shows acute inflammation
  • neutrophil migration

risk for fibrinous pericarditis with friction rub

38
Q

findings 3-14 days after MI

A

gross: hyperemic border; central yellow-brown softening (maximally yellow and soft by 10 days)

LM:
macrophage infiltration followed by granulation tissue at the margins

risk of free wall rupture –> tamponade, papillary muscle rupture, ventricular aneurysm, interventricular septal rupture due to macrophages that have degraded important structural components

39
Q

findings 2 weeks to several months after MI

A

gross: recanalized artery, region of infarct is gray-white

LM:
contracted scar is complete

risk for Dressler’s syndrome (AI fibrinous pericarditis 2/2 cardiac injury)

40
Q

cardiac troponin I

A

rises after 4 hours, elevated for 7-10 days

most specific protein marker for cardiac injury

41
Q

CK-MD

A

predominantly found in myocardium but can also be of skeletal muscle origin

***useful in diagnosing reinfarction after acute MI bc levels return to normal after 48 hours

42
Q

subendocardial infarcts

A

due to ischemic necrosis of

43
Q

EKG anterior wall LAD infarct

A

V1-4

44
Q

EKG anteroseptal LAD infarct

A

V1-2

45
Q

EKG anterolateral LCX infarct

A

V4-6

46
Q

EKG lateral wall LCX infarct

A

I, aVL

47
Q

EKG inferior wall RCA infarct

A

II, III, aVF

48
Q

Temporal arteritis

A

Large-vessel vasculitis

  • elderly female
  • u/l HA, jaw claudication
  • assoc. with PMR
  • tx w high-dose corticosteroid
49
Q

Takayasu’s arteritis

A

large-vessel vasculitis

-asian females

50
Q

polyarteritis nodosa

A

medium-vessel vasculitis

  • young adults
  • HBV in 30% of pts
  • p/w fever, weight loss, malaise, HA
  • GI sx = abd pain, melena
  • HTN, neuro dysfunction, cutaneous eruptions, renal damage
  • affects renal and visceral vessels, NOT PULMONARY ARTERIES
  • immune-complex mediated
  • transmural inflammation of the arterial wall with fibrinoid necrosis –> lesions of different ages
  • many aneurysms and constrictions on arteriogram
  • tx w/ corticosteroids and cyclophosphamide
51
Q

Kawasaki disease

A

medium-vessel vasculitis

asian children MI, rupture

tx - high dose aspirin and IVIG

52
Q

Buerger’s disease (thromboangiitis obliterans)

A

medium-vessel vasculitis

heavy smokers, males gangrene –> autoamputation of digits

  • superficial nodular phlebitis
  • Raynaud’s phenomenon
  • segmental thrombosing vasculitis

tx - STOP SMOKING

53
Q

microscopic polyangiitis

A

small-vessel vasculitis

necrotizing vasculitis commonly involving lungs, kidneys, skin with pauci-immune glomerulonephritis and palpable purpura

no granulomas
p-ANCA
tx with cyclophosphamide and corticosteroids

54
Q

Granulomatosis with polyangiitis (Wegener’s)

A

small-vessel vasculitis

upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis

lower respiratory tract: hemoptysis, cough, dyspnea

renal: hematuria, red cell casts

triad:

  1. focal necrotizing vasculitis
  2. necrotizing granulomas in the lung and upper airway
  3. necrotizing glomerulonephritis

c-ANCA
CXR- large nodular densities

tx with cyclophosphamide, corticosteroids

55
Q

Churg-Strauss syndrome

A

small-vessel vasculitis

Asthma, sinusitis, palpable purpura, peripheral neuropathy (wrist/foot drop)

can also involve heart, GI, kidneys (pauci-immune glomerulonephritis)

granulomatous, necrotizing vasculitis with EOSINOPHILIA

p-ANCA, elevated IgE

56
Q

Henoch-Schonlein purpura

A

small-vessel vasculitis

most common childhood vasculitis –> often after URI

Triad:

  1. skin: palpable purpura on buttocks/legs
  2. arthralgia
  3. GI: abd pain, melena, multiple lesions of same age

vasculitis 2/2 IgA complex deposition

associated with IgA nephropathy

57
Q

Bernard-Soulier syndrome

A

defect in GpIb receptor that binds platelets to vWF (which is attached to endothelium)

58
Q

Abciximab

A

blocks GpIIb/IIIa

59
Q

Glanzmann’s thrombasthenia

A

deficiency of GpIIb/IIIa

60
Q

Fibrinogen

A

links GpIIb/IIIa receptors

61
Q

causes of increased ESR

A

infections, AI disease, malignant neoplasms, GI disease, pregnancy

62
Q

causes of decreased ESR

A

polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia

63
Q

orotic aciduria

A

genetic mutation in UMP synthase –> can’t make uridine from orotic acid

p/w metaloblastic anemia not cured by B12 or folate

tx with uridine monophosphate to bypass defective enzyme

64
Q

causes of nonmegaloblastic macrocytic anemias

A

basically macrocytic anemia where DNA synthesis is not impaired

  • liver disease
  • EtOHism
  • reticulocytosis
  • drugs (5-FU, AZT, hydroxyurea)
65
Q

aplastic anemia

A

c/b failure or destruction of myeloid stem cells due to:

  • radiation and drugs (benzene, chloramphenicol, alkylating agents, antimetabolites)
  • viral agents (parvoB19, EBV, HIV, HCV)
  • Fanconi’s anemia (DNA repair defect)
  • idiopathic (immune-mediated, primary stem cell defect); may follow acute hepatitis

findings: hypocellular bone marrow with fatty infiltration

66
Q

AIP: defect, substrate accumulation, 5Ps, and tx

A

defective porphobilinogen deaminase

accumulation of porphobilinogen, ALA, uroporphyrin (urine)

  • Painful abdomen
  • Port wine-colored urine
  • Polyneuropathy
  • Psychological disturbances
  • Precipitated by drugs

Tx: glucose and heme (inhibit ALA synthase)

67
Q

PT tests…

A

extrinsic pathway

I, II, V, VII, X

68
Q

PTT tests…

A

intrinsic pathway

all factors except VII and XIII

69
Q

vitamin K cofactors

A

II, VII, IX, X, protein c, protein S

see inc in PT and PTT

70
Q

Glanzmann’s thrombasthenia

A

defect in platelet plug formation

dec GpIIb/IIIa –> defective platelet aggregation

Labs: blood smear shows no platelet clumping

71
Q

ITP

A

defect: anti-GpIIb/IIIa Ab —> splenic macrophage consumption of platelet/Ab complex

dec platelet survival –> low platelet count

labs: inc megakaryocytes

72
Q

TTP

A

deficiency in ADAMTS 13 (vWF metalloprotease) –> dec degradation of vWF multimers –> inc large vWF multimers –> inc platelet aggregation and thrombosis

dec platelet survival hence low platelets

labs; schistocytes, inc LDH

73
Q

TTP pentad of sx

A

neurologic, renal, fever, thrombocytopenia, microangiopathic hemolytic anemia

74
Q

vWF disease

A

dec platelet to vWF adhesion 2/2 low vWF

most common inherited bleeding d/o

AD

dx with ristocetin assay

tx: desmopressin (DDAVP) –> releases stored vWF from endothelium

75
Q

causes of DIC

A

“STOP Making New Thrombi”

Sepsis (gram-negative)
Trauma
Ob complications
acute Pancreatitis 
Malignancy
Nephrotic syndrome
Transfusion
76
Q

Factor V Leiden mx

A

mutant factor V resistant to degradation by protein C

most common inherited hypercoagulability in whites

77
Q

Prothrombin gene mx

A

mx in 3’ UTR –> inc production of prothrombin –> inc plasma levels and venous clots

78
Q

Antithrombin deficiency

A

inherited

inc PTT blunted after give heparin (bc it potentiates action of ATIII)

79
Q

Protein C or S deficiency

A

dec ability to inactivate factors V and VIII –> inc risk of thrombotic skin necrosis with hemorrhage following admin of warfarin (bc it inactivates C and S further)

80
Q

what is in fresh frozen plasma

A

coagulation factors

81
Q

what is in cryoprecipitate

A

fibrinogen, factor VIII, factor XIII, vWF, and fibronectin

82
Q

Most common Hodgkin’s lymphoma

A

nodular sclerosing

best prognosis

83
Q

Burkitt’s lymphoma genetic mutation

A

t(8;14) - translocation of c-myc on 8 and havey chain Ig (14)

affects adolescents and young adults

84
Q

Path findings of Burkitt’s, virus it’s associated with, endemic vs sporadic form

NHL

A

starry sky - sheets of lymphocytes with interspersed macrophages

associated with EBV

jaw lesion in endemic form in Africa; pelvis or abdomen in sporadic form

85
Q

most common adult non-hodgkin lymphoma

A

Diffuse large BC lymphoma

20% of mature TC origin

86
Q

Mantle cell lymphoma genetic mutation

A

t(11;14)

cyclin D1 (11) and heavy-chain Ig (14)

poor prognosis, CD5+

87
Q

Follicular lymphoma genetic mx

A

t(14;18)

heavy chain Ig (14) and bcl-2 (18)

difficult to cure, indolent course

88
Q

Adult TC lymphoma

A

c/b HTLV-1

p/w cutaneous lesions, esp affects Japan, West Africa and Caribbean

Aggressive

89
Q

Mycosis fungoides/Sezary syndrome

A

mature TC neoplasm

adults p/w cutaneous patches/nodules

CD4+, indolent course

90
Q

Multiple Myeloma

A

produces lots of IgG (55%) and IgA (25%)

most common primary tumor of bone in elderly

a/w primary amyloidosis, punched out lytic lesions, Monoclonal M protein spike, Ig light chains in urine (Bence Jones protein), rouleaux formation of RBCs

CRAB: hyperCalcemia, Renal insufficiency, Anemia, Bone lytic lesions/Back pain

91
Q

Waldenstrom’s macroglobulinemia

A

M spike = IgM (–>hyperviscosity symptoms); no lytic bone lesions

92
Q

MGUS

A

monoglonal gammopathy of undetermined significance

monoclonal expansion of plasma cells with M spike

asx PRECUROSR of MM –> develop MM 1-2% per year

Step 1 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions