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MQW U4 > Robbin's Qs > Flashcards

Robbin's Qs Flashcards

1
Q

In the cranial cavity, what vessels are most likely to be invaded by malignant cells within the vascular lumina?

  • -Arterioles
  • -Capillaries
  • -Lymphatics
  • -Muscular arteries
  • -Veins
A

–Veins – thin walls relative to diameter, less distinct layers, slow blood flow make them more prone to compression and invasion by malignancies. (route for hematogenous metastases)

–Lymphatics also, but not in cranial cavity

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2
Q

44 y/o woman w/ BP 150/100 has TIA. Labs: normal K, Na, nattriuretic peptide, increased plasma rening activity. Normal urinary Na excretion. What is most likely seen on renal arterial angiography?

  • -Arterial dissection
  • -AV fistula
  • -Berry aneurysm
  • -Focal stenosis and dilation
  • -Vascularized mass lesion
A

–Focal stenosis and dilation – Fibromuscular dysplasia (FMD) usually involves renal and carotids.

  • -FMD = HTN –> medium/large vessel thickening
  • -Renal stenosis –> RAAS activation
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3
Q

Dermal venule w/ endothelial cells is stressed by biogenic amines from mast cells following anaphylaxis. Extravascular fluid compartment increases in size. What is occuring in activated endothelial cells?

  • -Cytoplasmic contraction
  • -Free radical formation
  • -mRNA translation
  • -Thromboxane syntehsis
  • -VEGF elaboration
A

–Cytoplasmic contraction

–Anaphylaxis = exudation of intravascular fluid –> edema

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4
Q 
73 y/o healthy man has lightheadedness w/ episodes of fainting for 10 days. Exam: BP 135/90 lying down, 100/60 when sitting. Normal electrolytes. 
What BP regulatory mechanism is altered?
--Aldosterone release
--CO
--Intravascular volume
--Renin synthesis
--Sympathetic tone
--Vasoconstriction
A

–Intravascular volume

–Fluid loss or decreased fluid intake –> low volume –> orthostatic hypotension

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5
Q

55 y/o woman w/ dull, episodic headaches for past year. Exam: 37C, 166/112, P70, RR14. Lungs clear, HR regular. Abdom ultrasound: left kidney smaller than right. Renal angio: focal stenosis of L renal artery.
What is likely elevated lab finding?

A

–Plasma renin – 2ndary HTN = stenosis –> low GFR, low afferent arteriole pressure –> Renin release by juxtaglomerular cells –> Angiotension II-induced vasoconstriction –> high TPR –> higher volume

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6
Q 
Group of subjects w/ BP between 145/90 and 165/105. They have: increased CO, increased peripheral vascular resistance, normal renal angiogram, normal abdom C, normal serum creatinine and BUN, no meds. 
What is most likely lab finding?
--Decreased urine Na
--Elevated plasma renin
--Hypokalemia
--Increased urine catecholamines
--Lack of ACE
A

–Decreased urine Na – essential HTN = reduced Na homeostasis –> retained Na –> increase intravascular volume –> high CO –> compensation by increasing peripheral vascular resistance –> increased BP

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7
Q 
61 y/o woman w/ 2pk/day 40yr smoking Hx has increasing dyspnea for 6 years. Exam: 37.1C, P60, RR18 and labored, BP 130/80, expiratory wheezes bilaterally. CXR: increased lung volume, flattening of diaphragm, greater lucency to all lung fields, pulmonary artery prominence, prominent border on right sie of heart. Blood gas: PO2=80, PCO2=50, pH 7.35.
What is likely to be in pulmonary arteries?
--Amyloid deposition
--Atheromatous plaques
--Intimal tears
--Medial calcific sclerosis
--Necrotizing vasculitis
--Phlebothrombosis
A

–Atheromatous plaques – Obstructive/restrictive lung disease –> high pulm vascular resistance –> pulm HTN –> pulm atherosclerosis

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8
Q

Prevalence of essential HTN has increased for past 10 years to affect 1/4 of adults.
What lifestyle change can be adopted to decrease this?

A

– Lower dietary salt intake – Essential HTN = Na+ homeostasis dysfunction

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9
Q 
45 y/o man w/ poorly controlled HTN of up to 160/90 for 11 years has increased BP up to 250/125 for past 3 months. CXR: prominent border on L side of heart. Creatinine has increased from 1.7 to 3.8.
What happened?
What vascular lesion is most likely found?
--Fibromuscular dysplasia
--Granulomatous arteritis
--Renal arterial stenosis
--Necrotizing arteriolitis
--Polyarteritis nodosa
A

–Malignant HTN superimposed– hyperplastic arteriolosclerosis = arteriole concentric thickening –> luminal narrowing –> fibrinoid necrosis

–Necrotizing arteriolitis

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10
Q

57 y/o woman has mild intermittent right hip pain after falling down stairs. Exam: 3cm contusion over right hip, tender to palpation, full range of motion of right leg. XRay: calcified, medium-sized arterial branches in pelvis.
What is this vascular finding?

A

–Monckeberg arteriosclerosis = benign process, incidental finding.

–Often at distal extremities, pelvis, thyroid, breast regions

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11
Q

20 year old men and women are assessed for development of atherosclerotic cardiovascular disease. What lab result finding is most likely to indicate the greatest relative risk for development of disease?

  • -Anti-proteinase3
  • -CRP
  • -Cryoglobulin
  • -ESR
  • -Platelets
A

–CRP = acuse phase reactant that increases in response to inflammation

–ESR is nonspecific indicator of inflammation

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12
Q

35 y/o woman has angina pectoris for 6mo. Exam: BP 135/85. 5ft 5in, 82kg (BMI29). HbA1C 9%, fasting glucose 143. Coronary angio = 75% narrowing of LAD, 70% narrowing of RCA.
What is her greatest risk factor for atherosclerotic disease?

A

–Diabetes Mellitus – her HbA1C and glucose suggests hyperglycemia.

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13
Q

In early atheroma develpment, monocytes attach to endothelium, migrate subendothelially, become macrophages and then transform into foam cells
What substance is responsible for macrophage transformation?

A

–Oxidized LDL – taken up by “scavenger” pathway in macrophages –> transform to foam cells –> form fatty streak.

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14
Q

29 y/o man has angina for past year. Family Hx of CV disease. BP 120/80. Total cholesterol 185, glucose 85.
Mutation in gene encoding for what is most likely in this man’s family?

A

–Apolipoprotein – Lipoprotein(a) = altered form of LDL cholesterol w/ apoB-100 of LDL linked to apolipoprotein A.

–Increased Lp(a) –> risk for endothelia dysfunction and atherogenesis

–Statin drugs affecting LDL receptor does not affect Lp(a) concentration.

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15
Q

Study of subjects w/ LDL over 160 found to have increased oxidized LDL and decreased arterial lumen size.
What is most likely initial pathologic change arterial narrowing?

A

–Intimal thickening – initial injury response = intimal thickening w/ neointimal smooth muscle cell proliferation and production of increased intimal ECM

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16
Q

50 y/o man w/ 2yr Hx of angina pectoris during exercise. BP 135/75, HR79 and slightly irregular. Coronary angio: fixed 75% narrowing of LAD. Atherosclerosis risk factors: smoking, HTN, HCL. What is earliest event in atherosclerotic disease?

A

–Endothelial injury – Atherosclerosis = initial endothelial injury –> subsequent chronic inflammation –> repair of arterial intima

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17
Q

You do an aortic biopsy of a child over the age of 10 and see fatty streaks.
What cells do you find (which is only present early in the pathogenesis of atherosclerotic lesions)?

A

–T lymphocytes – believed to activate monocytes, endothelial cells, and smooth muscle cells by secreting cytokines.

–Adhere to VCAM-1 on activated endothelial cells and migrated into the vessel wall

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18
Q

Release of groth factors (PDGF, FGF, TNF-a) lead to increased ECM production, causing atheromatous plaque size increase.
Which cells release these growth factors in plaques?

A

–Smooth muscle – activated platelets, macrophages, and vascular wall cells release growth factors –> smooth muscle cell recruitment –> micration from media to intima –> proliferate –> synthesize ECM

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19
Q

58 y/o woman has chest pain at rest for past year. Pulse 80 and irregular. LAD lumen is markedly narrowd by atheromatous plaque complicated by calcification.
Wat is most likely involved in pathogenesis?
–Elevated platelets
–Low HDL
–Low Lp(a)
–Low plasma homocysteine
–Positive VDRL

A

–Low HDL – atherogenesis risks = HCL w/ high LDL and low HDL

–VDRL –> syphilis

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20
Q

What kind of plaque alterations is least likely to be associated w/ acute coronary syndromes?

  • -Calcium deposition
  • -Hemorrhage into plaque substance
  • -Intermittent platelet aggregation
  • -Thinning of media
  • -Ulceration of plaque surface
A

–Thinning of media – expanding plaque compresses the media –> cause thinning –> weak wall –> predispose to aneurysm formation

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21
Q

59 y/o woman w/ DM2 has an episode of chest pain with exercise. BMI=30, angiography: proximal coronary 70% stenosis. What daily low dose pharmacologic agent is most appropriate for reducing her myocardial infarction risk?

A

– Aspirin (acetylsalicylic acid) – inhibids COX pathway

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22
Q 
84 y/o man w/ long smoking Hx survived a small MI 2 years ago. Now has chest and leg pain on exercise. T37.1, P81, RR15, BP 165/100. Poor peripheral pulses in lower extremities. 7cm pulsating mass in midline lower abdomen. Fasting glucose between 170-200.  
What vascular lesion does he most likely have?
--Aortic dissection
--AV fistula
--Atherosclerotic aneurysm
--Polyarteritis nodosa
--Takayasu arteritis
--Thromboangiitis obliterans
A

–Atherosclerotic aneurysm – abdom aneurysm related to underlying aortic atherosclerosis

  • -AV fistula = audible bruit on auscultation
  • -Takayasu = aortic branches, children
  • -Thromboangiitis obliterans = Buerger, smoker, lower extremities
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23
Q

41 y/o man has worsening abdom pain for past week. T36.9, P77, RR16, 140/90. Abdom CT: 6cm diameter enlarged abdom aorta.
What is most likely underlying disease process?
–Diabetes mellitus
–Marfans
–Polyarteritis nodosa
–SLE
–Syphilis

A

–Diabetes Mellitus – important risk factor for atherosclerosis in younger men/premenopausal woman

  • -Marfan = dilated ascending aorta
  • -PAN = not aorta
  • -SLE = small arteriolar vasculitis
  • -Syphilis = thoracic aorta
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24
Q

77 y/o man w/ progressive dementia and gait ataxia for 8 years succumbs to bronchopneumonia. Autopsy: thoracic aorta has dilated root and arch, intimal “tree-bark” appearance. Micro: obliterative endarteritis of vasa vasorum.
What is it?

A

Syphilitic Aortitis – classic “tree-bark appearance in thoracic aorta and obliterative endarteritis; affect vasa vasorum

–Hx: tabes dorsalis (ataxia), neursyphilis (dementia)

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25
Q

23 y/o man with sudden onset severe, sharp chest pain. T36.9, lungs clear. CXR: widened mediastinum. TEE: dilated aortic root and arch w/ tear in aortic intima 2cm distal to great vessels.
What does he have?

A

–Marfan syndrome – disruption of medial elastic fibers (cystic medial degeneration) –> weakens aortic media –> risk for dissection

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26
Q

59 y/o man w/ sudden severe chest pain radiating to back. BP 170/110, distant heart sounds. Pulsus paradoxus (abnormally large decrease in SBP during inspiration) observed.
What is it?

A

–Aortic dissection – sudden tear of proximal aortic intima –> blood enters space between layers –> enters pericardial cavity –> cardiac tamponade

  • -blood entering chest cavity –> hemothorax
  • -HTN is most common risk factor for dissection
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27
Q

75 y/o man has headaches for past 2 months. T37, P68, RR15, 135/85. Right temporal artery prominent, palpable, and painful to touch. ESR 100, temporal artery biopsy shows grossly thickened and focal microscopic granulomatous inflammation. Responds to corticosteroid therapy.
What is the most likely complication in untreated patients?

A

– Blindness – Giant cell (temporal) arteritis = large-medium external carotid branches, but also vertebral and ophthalmic arteries.

–associated w/ polymyalgia rheumatica

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28
Q 
32 y/o woman has coldness and numbness in arms and decreased right eye vision for 5 months. Afebrile, 100/70, non-palpable radial pulses, strong femoral pulses, decreased sensation and cyanosis in arms, no warmth or swelling. CXR: prominent right side heart border, pulmonary artery prominence. Glucose 74, creatinin 1, cholesterol 165, negative ANA. Stable condition for the next year
What is it? 
--Aortic dissecition
--Kawasaki
--Microscopic polyangiitis
--Syphilis
--Takayasu
--Thromboangiitis obliterans
A

–Takayasu arteritis – “pulseless disease”, involves aortic arch

  • -Kawasaki = children, acute febrile, coronary arteritis, rash
  • -
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29
Q 
43 y/o man has malaise, fever, 4kg weight loss over past month. 145/90, mild diffuse abdom pain, no mass or hepatosplenomegaly. BUN 58, creatinin 6.7, Renal angiography: right renal arterial thrombosis, left renal artery and branches narrow w/ focal aneurysmal dilation. During hemodialysis: abdom pain, diarrhea, melena.
What is most likely lab finding?
--ANA
--C-ANCA
--HIV
--HBsAg
--Scl-70
--RPR
A

–HBsAg – classic Polyarteritis nodosa (PAN) = segmental involvement of medium-sized arteries w/ aneurysmal dilation in renal and mesenteric vascular beds

  • -ANA = SLE
  • -Scl-70 = scleroderma
  • -RPR = syphilis
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30
Q

3 y/o from Osaka japan has fever, rash, swelling of hands and feet for 2 days. T37.8, desquamative skin rash, oral erythema, cervical lymphadenopathy. Improves w/ IVIg therapy.
What is a complication of untreated disease?
–Asthma
–Intracranial hemorrhage
–Glomerulonephritis
–MI
–Pulmonary HTN

A

–MI – Kawasaki disease = 20% cardiovascular complications (thrombosis, ectasia, coronary aneurysm)

  • -Asthma = Churg-Strauss
  • -Glomerulonephritis = ANCA associated, SLE
  • -Pulmonary HTN = Takayasu
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31
Q

50 y/o man has chronic cough for 18 months. Exam: nasopharyngeal ulcers, diffuse crackles bilat., BUN 75, creatinine 6.7. Urinalysis = 50RBCs/field, RBC casts. C-ANCA (proteinase 3) elevated. CXR: multiple, small, bilateral pulmonary nodules. Biopsy: necrotizing inflammatory processes of small peripheral pulm. arteries and arterioles.
What is it?

A

–Granulomatosis w/ polyangiitis – ANCA associated vasculitis = hypersensitivy reaction, small-medium vessels

–C-ANCA in 90% of cases

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32
Q

50 y/o man with muscle pain and fever for a month has darker colored urine for 2 weeks. Palpable purpuric lesions on skin. Urinalysis: hematuria, proteinuria. Lab: mixed cryoglobulinemia w/ polyclonal IgG increase, high P-ANCA.
What is most likely finding in skin biopsy?
–Giant cells and macrophages
–Medial fibrinoid necrosis
–Microabscesses
–Mycotic aneurysms
–Perivascular eosinophilic infiltrates

A

–Medial fibrinoid necrosis – Microscopic polyangiitis = small vessels (capillaries), commonly kidney and lungs

  • -Microabscesses = infectious or Buerger disease
  • -Perivascular eosinophilic infiltrates = Churg-Strauss
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33
Q

33 y/o man w/ 2pk/day smoking Hx since teenager has painful thromboses of superficial veins of lower legs for 1 month w/ episodes of fingers becoming blue and cold. Next year, he develops ppor healing ulcerations on feet, one toe gangrenous and amputated. Histo: acute chronic vasculitis of medium-sized arteries w/ segmental invovlement.
What is most appropriate treatment?

A

–Smoking cessation – Buerger disease (Thromboangiitis obliterans = small-medium arteries of extremities, associated w/ smoking. eventually involves peripheral veins and nerves

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34
Q

8 y/o child has abdom pain and dark urine for 10 days. Exam: blotchy purple skin lesions on trunk and extremities. Urinalysis: hematuria, proteinuria. Negative P-ANCA and C-ANCA. SKin biopsy: necrotizing vasculitis of small dermal vessels. Renal biopsy: immune complex deposition in glomeruli w/ IgA-rich immune complexes.
What is it?

A

–Henoch-Schonlein purpura = in children, IgA nephropathy

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35
Q

35 y/o woman w/ HX of injection drug use has fever for 1 day. T37.6, heart murmur, culture grows S. aureus. Develops severe headache. Head CT: intracranial hemorrhage.
Which vascular complication most likely occurred in her brain?
–Bacillary angiomatosis
–Hyperplastic arteriolosclerosis
–Lymphangitis
–Mycotic aneurysm
–Phlebothrombosis

A

–Mycotic aneurysm – infectious endocarditis –> vegetation dislodge and embolize –> local arterial destruction

–Bacillary angiomatosis = focal vascular proliferation, skin, immunocompromised, Bartonella

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36
Q 
60 y/ woman has paleness on tip of middle finger when driving to work one day associated w/ pain and numbness. Resolves 20min after entering warm office building. 
What pathologic process?
--Calcification
--HTN
--Thrombosis
--Vasculitis
--Vasoconstriction
A

–Vasoconstriction – Raynaud phenomenon = “red, white, and blue” changes, primary exaggerated vasoconstriction

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37
Q 
21 y/o woman in 34th wk of pregnancy has itching and burning pain in perianal region for past 4 months. Small amount of bright red blood on toilet paper last week. 
Which condition is most likely?
--Filariasis
--Polyarteritis nodosa
--External hemorrhoids
--Micronodular cirrhosis
--Rectal adenocarcinoma
A

–External hemorrhoids – venous congestion –> dilated hemorrhoidal veins.

–Filarial infections = lymphatics–> lymphadema

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38
Q

69 y/ o woman bedridden from viral pneumonia complicated by baterial pneumonia for past 2 weeks. Exam: swelling, tenderness of right leg, worses when raising or moving leg.
What is it?

A

–Thrombosis of Deep veins – Phlebothrombosis = venous stasis w/ prolonged immobilization.

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39
Q 
54 y/o woman has increasing prominence of dilated superficial veins over both lower legs for past 5 years. T37, P70, RR14, 125/85. No pain, swelling, or tenderness.
What is most likely consequence?
--Atrophy of lower leg muscles
--DIC
--Gangrenous necrosis of lower legs
--Pulmonary thromboembolism
--Stasis dermatitis w/ ulceration
A

–Stasis dermatitis w/ ulceration – Chronic peripheral venous stasis –> hemosiderin deposition and dermal fribrosis w/ brownish discoleration and skin roughening –> focal ulceration over varicosities

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40
Q

48 y/o woman develops persistent swelling and puffiness in left arm after mastectomy w/ axillary node dissection for breast cancer 1 yr ago. Develops left arm cellulitis 3 months ago. Exam: firm skin and “doughy” underlying soft tissue, not painful or discolored.
What is it?

A

–Lymphadema – obstruction of lymphatics in axilla –> lymphadema –> cellulitis complication

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41
Q

50 y/o man cuts his right index finger on metal shard while cleaning debris in an irrigation canal. Bleeding stops in 3 min, but 6 hours later, he has pain. T38C, red streaks from right hand to upper arm, arm swollen and tender, tender lumps in right axilla. Cultures grow group A B-hemolytic strep.
What is it?

A

–Lymphangitis – classic red streaks indicate acute infection draining to axillary lymph nodes

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42
Q

46 y/o man has increasing abdom enlargement over 15 months. Exam: multiple skin lesions on upper chest w/ central pulsatile cores and radius 0.5-1.5cm. Pressing core causes radially arranged array of subcutaneous arterioles to blanch. Glucose 112, creatinine 1.1, total protein 5.8, albumin 3.4. What is likely underlying disease?

  • -AIDS
  • -Diabetes Mellitus
  • -Granulomatosis w/ polyangiitis
  • -Marfan syndrome
  • -Micronodular cirrhosis
A

–Micronodular cirrhosis –characteristic spider telangectasias, consequence of chronic alcohol abuse

–Thought to be caused by hyperestrogenism from reduced clearance

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43
Q

21 y/o woman in 3rd trimester has enlarging nodule in mouth for 2 weeks. Exam: 1cm red nodule on left lateral gigiva below first molar. Regresses after delivery.
What is it?

A

–Capillary hemangioma – pyogenic granuloma

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44
Q

10 y/o boy has 2cm spongy, dull red, circumscribed lesion on upper outer left arm present since infancy w/o change. excised biopsy: dilated, endothelium-lined spaces filled w/ RBCs.
What is it?

A

–Hemangioma

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45
Q 
6 y/o has increasing neck size for past year. Exam: ill-defined, soft mass deforming left side of his neck. Resection of 10cm mass examined: borders not discrete, dilated spaces filled w/ milky fluid, bounded by thin connective tissue walls. Spaces lined by flattened endothelium, surrounded by collagenous tissue and smooth muscle w/ collections of small lymphocytes. 
What is most likely outcome?
--Distant metastases
--Local rucurrence
--More neoplasms elsewhere
--Opportunistic infection
--Sarcomatous transformation
A

–Local recurrence – Cavernous lymphangioma = histologically benign, tend to become large and extend around adjacent structures

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46
Q

35 y/o man w/ HIV for 10 years has multiple reddish, purple, nodular skin lesions that slowly increasing for the past year. What likely played role in development of this?

  • -Antiretroviral therapy
  • -EBV
  • -Hyperlipidemia
  • -Mycobacterium avium complex infection
  • -Sexual intercourse
A

–Sexual intercourse – Kaposi sarcoma = caused by HHV8 infection, STD

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47
Q

67 y/o woman w/ glucose intolerance, HTN, central obesity, HCL has increasing dyspnea from worsening CHF. Echo: EF 25%. Stent placed containing Paclitaxel. What long-term complication is prevented by paclitaxel?

A

–Proliferative restenosis – intimal thickening following angioplasty –> restenosis; paclitaxel limits smooth muscle hyperplasia

–Metabolic syndrome = coronary atherosclerosis risk

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48
Q

82 y/o woman has increasing fatigue for 2 years with paroxysmal dizziness and syncope. Afebrile, Pulse 44, RR 16, 100/65, lungs clear, no murmurs. Echo: normal size heart, normal valve motion, EF 50%. Vagal stimulation slows heart rate and becomes irregular. Abnormality where is most likely?

A

–SA node – Bradycardia less than 50/min suggests SA disorder

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49
Q 
Neonate at newborn checkup has systolic murmur. Echo: muscular defect of intraventricular septum. Checkup 30 years later shows no murmur or flow defect. 
What kind of cells proliferated leading to disappearance of defect?
--Adipocytes
--Conduction cells
--Endothelial cells
--Fibroblasts
--Mesothelial cells
--Stem cells
A

–Stem cells – stems cells most active in neonates

  • -Adipocytes enlarge with aging
  • -Endothelial cells make more coronary collateral channels
  • -Fibroblasts produce collagenous scars reducing contractility
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50
Q

66 y/o man has cough and worsening SOB for 3yrs. Dullness to percussion bilat lung bases, poor audible breath sounds, P77, BP110/80, no angina, liver span increased to 14cm, pitting edema to knees, JVD to angle of jaw.
What most likely caused his heart disease?

A

–Smoking – right-sided CHF –> edema, pleural effusion, hepatic congestion, JVD

–Right side CHF most often follows COPD = cor-pulmonale

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51
Q 
62y/o woman has increasing dyspnea for 2 years. Now wakens at night w/ air hunger, cough w/ frothy sputum. Rales (crackles) in all lung fields, PMI strong and displaced laterally. Echo: EF30%, concentric LV wall size.
What underlying disease does she have?
--Amyloidosis
--Cardiomyopathy
--HTN
--Myocarditis
--Pericarditis
A

–HTN – left-sided CHF –> pulm. congestion and edema.

–Systemic HTN –> high pressure (afterload) –> concentric LVH w/ systolic dysfunction

–Other choices cause diastolic dysfunction

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52
Q 
41 y/o woman wakens night w/ air hunger for past year. Sleeps better when sitting in bed. Serum B-type natriuretic peptide > 400 (v high).
What cardiac disease best explains this?
--Atrial myxoma
--Fibrinous pericarditis
--Giant cell myocarditis
--Libman-Sacks endocarditis
--Rheumatic valvulitis
A

– Rheumatic valvulitis – paroxysmal nocturnal dyspnea = Rheumatic disease affects Aortic or Mitral valves most likely –> L-side CHF –> pulm. edema

  • -Myxoma = intermittent obstruction
  • -Fibinous pericarditis = chest pain, small amount of fluid
  • -Giant cell myocarditis = rare
  • -Libman-Sacks = in SLE, not impair valve or ventricular fxn
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53
Q

50 y/o man has increasing abdom discomfort and leg swelling for 2 years. Smoked for 35 years, JVD even when sitting, large tender liver palpable 10cm below costal margin, pitting edema in lower extremities. CXR: bilat. diaphragmatic flattening, pleural effusions, increased lucency of lung. Thoracentesis: 500mL clear fluid w/ few cells.
What is it?

A

–Chronic bronchitis – Obstructive lung disease (emphysema) –> pulm HTN –> R-side heart failure

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54
Q 
Infant has cyanosis during 1st week of life and a heart murmur. Echo: overriding aorta, VSD, r-ventricular thickening, pulm. stenosis.
Inherited mutation in what gene?
--B-myosin heavy chain (B-MHC)
--Fibrillin 1 (FBN1)
--KCNQ1
--NOTCH2
--Transthyretin (TTR)
A

–NOTCH2 – Tetralogy of Fallot

  • -B-MHC = hypertrophic cardiomyopathy
  • -FBN1 = Marfan
  • -KCNQ1 = long QT syndrome
  • -TTR = one form of cardiac amyloidosis
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55
Q

Infant from uncomplicated pregnancy is normal at birth, but develops resp. distress at 1 day. Tachypnic, tachycardic, cyanotic, S1 ejection click, split S2 w/ prominent P sound. CXR: normal heart size, prominent hilar vascular markings. Echo: small L atrium, large R atrium, normal ventricles, patent foramen ovale, normal aorta and pulm trunk position.
What congenital heart disease?
–ASD
–Coarctation of aorta, preductal type
–PDA
–Tetralogy of Fallot
–Total anomalous pulmonary venous connection

A

–Total anomalous pulmonary venous connection – pulmonary veins leading to right atrium instead of left

  • -ASD = not enough
  • -Coarctation = no cyanosis, preductal form life-threatening
  • -PDA = no cyanosis
  • -Tetralogy = overriding aorta
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56
Q

77 y/o woman fell and fractured ankle, bedridden for 16 days. Develops sudden chest pain, dyspnea, diaphoresis. L thigh swelling, tenderness. Chest CT: areas of decreased attenuation in right and left pulm arteries. 1 day later: difficulty speaking. MR angiography: L MCA occlusion.
What cardiac abnormality does she have?

A

–PFO (Patent Foramen Ovale) –DVT –> PE, moves to left heart through shunt –> “paradoxical embolus” –> stroke

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57
Q

5 y/o child not as active as other children. Past 8 months: multiple episodes of resp. difficulty following exertion. T37, P81, RR19, 95/60, loud holosystolic murmur, diffuse crackles bilat., dullness to percussion at bases. CXR: prominent L heart border, pulm. interstitial infiltrates, blunting of costodiaphragmatic recesses. Large VSD seen.
What additional pathologic conditions will he develop?
–Aortic regurg
–Coronary atherosclerosis
–Nonbacterial thrombotic endocarditis
–Pulm HTN
–Restrictive cardiomyopathy

A

–Pulm HTN – large VSD uncorrected by age 5 –> marked L to R shunting –> pulm HTN (Eisenmenger complex)

–Ventricle chambers undergo hypertrophy and some dilation

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58
Q 
3 y/o  developing normally has low-pitched cardiac murmur. Echo: present ostium secundum w/ 1cm defect.
Which abnormality is most likely?
--Cyanosis at rest
--L-->R shunt
--Mural thrombosis
--Pericardial effusion
--Pulm HTN
A

–L–>R shunt – persistent ostium secundum is most common ASD; low atrial pressures = small amount of shunting

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59
Q

2 y/o w/ Staph. epidermidis illness 1 year ago given abx and recovered. Now on exam: harsh, waxing and waning, machinery-like murmur at upper chest. CXR: prominence of pulm. arteries. Echo: normal valves. Normal arterial O2
What congenital heart disease explains these findings?
–Aortic atresia
–Aortic coarctation
–ASD
–PDA
–Tetralogy of Fallot

A

–PDA – L–>R shunting; can produce significant murmur and predispose to infection; pulm arteries prominence = pulm HTN

  • -Atresia = hypoplastic L heart, no survival
  • -Coarctation = no shunting, no pulm HTN
  • -ASD = no loud murmur
  • -Tetralogy = pulm stenosis –> no pulm HTN, R–>L shunt
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60
Q 
5 y/o girl below 5percentile in height and weight has easy fatigability since infancy. Cyanotic, T37, P82, RR16, 105/65, pulse ox shows decrease O2 sat. 1 month later: fever, obtundation. Cerebral CT: right parietal, ring-enhancing, 3cm lesion.
What congenital heat disease?
--ASD
--Bicuspid aortic valve
--Coarctation of aorta
--PDA
--Truncus arteriosis
--VSD
A

–Truncus arteriosis – Cyanosis = R–>L shunt

–Cyanotic heart disease most commonly caused by: truncus arteriosis, transposition of great arteries, and tetralogy of Fallot.

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61
Q

Studying tetralogy of Fallot, some have more severe CHF, poor exercise tolerance, and decrease arterial O2 sat.
What predicts worse clinical presentation?
–Degree of pulm. stenosis
–Diameter of tricuspid valve
–Presence of ASD
–Size of VSD
–Thickness of L ventricle

A

–Degree of pulm. stenosis –mild stenosis –> VSD like symptoms (L–>R shunt, no cyanosis); severe stenosis –> R–>L shunt –> cyanotic heart disease

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62
Q

15 y/o boy complains of leg pain when running more than 300m. T36.8, P76, RR22, 165/90. Radial pulses 4+, dorsalis pedis pulse 1+, ABG shows normal O2. What congenital anomaly most likely?

  • -Aortic valve stenosis
  • -Coarctation of aorta
  • -PDA
  • -Transposition of great arteries
  • -Tricuspid valve atresia
A

–Coarctation of aorta – abnormal narrowing of aorta –> large pulse differences in upper vs lower extremities

–Collaterals supplying lower extremities often involve intercostal arteries –> enlarging arteries produce “rib notching” in CXR

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63
Q 
Infant develops respiratory distress and cyanosis 1 day after birth. Echo: slitlike L ventricle, small L atrium, atretic aortic and mitral valves.
What structure could blood from lungs most likely have reached systemic circulation
--Anomalous venous return
--Foramen ovale
--PDA
--Right 4th aortic arch
--Truncus arteriosus
--VSD
A

–PDA – infant has hypoplastic L heart syndrome; lung blood –> L atrium –> foramen ovale –> R atrium –> pulm trunk –> PDA –> aorta –> systemic circulation

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64
Q

60 y/o man has angina on exertion for 6yrs. Coronary angio 2yrs ago: 75% L circumflex, 50% RCA stenosis. Past 3 weeks: more frequent and severe anginal attacks, sometimes even when lying in bed. BP110/80, P85 w/ irregular beats. ECG: ST elevation. Lab: glucose 188, creatinine 1.2, toponin I 1.5.
What explains this?

A

–Atheromatous plaque fissure w/ thrombosis – causes unstable angina

65
Q

37 y/o woman has sudden onset chest pain. Exam: afebrile, tachycardic, hypotensive. ECG: ST elevation, pathologic Q waves. L circumflex artery completely occluded.
What is most likely underlying condition?
–Acute myelogenous leukemia
–Chronic alcoholism
–Diabetes mellitus
–Marfan syndrome
–Polyarteritis nodosa

A

–Diabetes mellitus – When pre-menopausa woman develops severe atherosclerosis–> think underlying diabetes or lipid disorder

  • -Chronic alcoholism = less atherosclerosis
  • -Marfan = cystic medial necrosis of aorta
66
Q 
56 y/o man has episodes of severe substernal chest pain on exercise worsening over past year, relieved by sublingual Nitroglycerin. Afebrile, P78 and regular, no murmurs of gallops. Creatinine 1.1, glucose 130, total cholesterol 223. 
What cardiac lesion most likely present?
--Calcific aortic stenosis
--Coronary atherosclerosis
--Rheumatic mitral stenosis
--Serous pericarditis
--Viral myocarditis
A

–Coronary atherosclerosis – angina pectoris occurs when coronary narrowing exceeds 75%

  • -aortic calcification = leads to L-sided CHF
  • -
67
Q

Studying MIs, a pattern of injury involving posterior L ventricular wall most likely caused by:

  • -Ascending aortic dissection
  • -LAD arterial plaque rupture
  • -L circumflex arterial vasculitis
  • -Right coronary sinus embolization
  • -Right posterior descending arterial thrombosis
A

–Right posterior descending arterial thrombosis – Posterior L ventricle and septum supplied by posterior descending artery (typically off RCA, can be off L circumflex)

–L circumflex supplies lateral L ventricle wall

68
Q 
48 y/o woman has increasing dyspnea for 2 days and experiences sudden cardiac arrest. L ventricle free wall histology shows eosinophilic myocardial fibers w/ loss of nuclei indicating coagulative necrosis and present contraction bands. 
What is the diagnosis?
--Acute rheumatic myocarditis
--Cardiomyopathy
--Myocardial infarction
--Septic embolization
--Viral myocarditis
A

–Myocardial Infarction –

69
Q

Hemorrhage and contraction bands in necrotic myocardial fibers are most likely to be seen with infarction in which of the following settings?

  • -Acute coronary vasculitis
  • -Anti-arrhythmic drug usage
  • -Angioplasty w/ stent placement
  • -Septic embolization
  • -Thrombolytic therapy
A

–Thrombolytic therapy – reperfusion of ischemic myocardium –> mitochondrial dysfunction –> leakage of blood and exaggerated contraction from Ca influx

70
Q

50 y/o man w/ diabetes and HTN has pain in L shoulder and arm for 12hrs. Next 6hrs: develops SOB persist for 2days. Day3 exam: 37.1, P82, RR18, 160/100. Lab: normal CK, elevated troponin I. Continued dyspnea for 3days. Day7: cardiac arrest and resuscitated. Imaging: large fluid collection around heart.
What complication developed?

A

–Hemopericardium – risk of myocardial rupture is greates 4-7 days after transmural myocardial necrosis

–CK normalizes in 72hrs, Troponin remains high for 7-10 days

71
Q

45 y/o man has crushing substernal chest after arriving at work. Next 4hrs: pain persists, radiate to L arm, becomes diaphretic, SOB. Waited 8hr to go to hospital.
Serum elevation of what lab test value is most useful for diagnosis?

A

–CK-MB fraction –most specific for acute MI, increases within 2-4 hours of ischemic myocardial injury

–LDH1 suggest myocardial injury, but peaks 3 days later

72
Q

19 y/o man suddenly collapses and brought to ED. 37.1, P84, RR17, 80/40. Lab: Hb 13.5, Plt 252k, WBC 7230, glucose 73, creatinine 1.2, total CK elevated, CK-MB fraction 10%.
What underlying condition is likely present in this patient?
–DiGeorge syndrome
–Down syndrome
–Familial hypercholesterolemia
–Hereditary hemochromatosis
–Marfan syndrome

A

–Familial hypercholesterolemia – CK-MB fraction indicates acute MI

73
Q 
69 y/o man w/ metabolic syndrome (3+ of: obesity, HTN, high glucose, high TG, low HDL) had chest pain and elevated Troponin I 1yr ago. Treated w/ anti-arrhythmics for 1wk. Echo: EF28%. Now has reduced exercise tolerance T37, P68, RR17, 130/80, diffuse crakles of lungs. He has an enlarged and dilated heart w/ a large ventricular aneurysm. 
What complication of disease is patient most likely to develop?
--Atrial myxoma
--Cardiac tamponade
--Constrictive pericarditis
--Hypertrophic cardiomyopathy
--Infective endocarditis
--Systemic thromboembolism
A

–Systemic thromboembolism – aneurysm from previous MI allows for stasis and turbulence, increasing risk for mural thrombus

74
Q

72 y/o man w/ poorly controlled diabetes, worsening exercise tolerance for 5yrs, chest pain w/ minimal exertion for past year. Bilat. pulmonary rales, pitting edema of legs, irregular heart beat. CXR: prominent right and left heart borders. Echo: EF25% w/ diminished walll motion. Lab: elevated B-type natriuretic peptide.
What pathological finding is most likely present?
–Critical coronary stenosis
–L atrial mural thrombus
–Hypertrophic cardiomyopathy
–Mitral and tricuspid valve thickening
–Pericardial fibrinohemorrhagic exudate

A

–Critical coronary stenosis – Ischemic heart disease b/c of Hx of diabetes and chest pain

75
Q 
68 y/o woman has increasing dyspnea and orthopnea for past year w/o chest pain. T37, P77, RR20, 140/90, diffuse crackles in all lung fields, no murmurs or gallops, regular heart rate. Coronary angio: 90% LAD stenosis. Echo: normal valves, decreased LV wall motion, EF32%. Glucose 81, creatinine 1.6, troponin I 1. 
What phramacologic agent would benefit this patient?
--Amiodarone
--Alteplase
--Glyburide
--Nitroglycerin
--Propranolol
--Simvastatin
A

–Simvastatin – She doesn’t have acute coronary syndrome, but does have major risks

  • -Amiodarone = for arrhythmias
  • -Glyburide = for type 2 diabetes
  • -Nitroglycerin = vasodilator for angina
  • -Propranolol = for HTN, can exacerbate bradycardia and CHF
76
Q

50 y/o man has sudden onset sever substernal chest pain radiating to neck. Afebrile, tachycardic, hyperventilaing, hypotensive, no cardiac murmurs. Coronary angio: thrombotically occluded L circumflex, 50-70% proximal circumflex and LAD.
What complication is most likely to occur in 1hour?
–Myocardial rupture
–Pericarditis
–Valvular insufficiency
–Ventricular fibrillation
–Thromboembolism

A

–Ventricular fibrillation – Immediately after coronary thrombosis, arrhythmia can lead to sudden cardiac death

–All others occur several days later

77
Q

In study of EMS patients, 5% w/ sudden cardiac arrest receiving CPR survive. What is most likely mechanism for cardiac arrest in these survivors?

  • -Arrhythmia
  • -Infarction
  • -Inflammation
  • -Valve failure
  • -Ventricular rupture
A

–Arrhythmia – most common cause of sudden cardiac cause is ischemic heart disease, but the first EVENT in ACS is typically arrhythmia, so resuscitation at this stage can be successful

78
Q 
59 y/o man has chronic fatigue for 18months. CXR: bilat. pulm edema, prominent L heart border. Glucose 74, total cholesterol 189, total protein 7.1, albumin 5.2, creatinine 6.1 BUN 58. Heart gross appearance show concentric LV hypertrophy. 
What is diagnosis
--Chronic alcoholism
--Diabetes mellitus
--Hemochromatosis
--Pneumoconiosis
--Systemic HTN
A

–Systemic HTN – HTN –> increased pressure load, often associated w/ chronic renal disease –> LV failure –> pulm edema

  • -Chronic alcoholism = associated w/ dilated cardiomyopathy
  • -Hemochromatosis = leads to dilated cardiomyopathy
  • -Pneumoconioses = restrictive lung disease, cor pulmonale, RVH
79
Q

56 y/o man has worsening cough and orthopnea for 2yrs. Dullness to percussion at both lung bases, diffuse crackles in upper lung fields, afebrile. Echo: marked LVH, severe aortic stenosis. Gross appearance of heart shows an aortic valve with some calcification and only 2 leaflets.
What underlying condition accounts for this?
–Congenital anomaly
–Diabetes mellitus
–Infective endocarditis
–Marfan syndrome
–Systemic HTN

A

–Congenital anomaly – bicuspid aortic valve –> tendency to calcify, leading to stenosis, LVH and L-side heart failure w/ pulm edema

–Bicuspid valve symptoms appear by age 50-60

80
Q 
73 y/o woman had an episode of disorientation, difficulty speaking, and persisting weakness of right side of body. Afebrile, P68, RR15, 130/85, lungs clear, irregular heart rate, midsystolic click. Chest CT: focus of bright attenuation in heart. Echo: one valvular leaflet appears to ballon up, EF55%. CK 100, glucose 77, creatinine 0.8, calcium 8.1, phosphorus 3.5. 
What is most likely diagnosis
--Carcinoid heart disease
--Hyperparathyroidism
--Infective endocarditis
--Mitral annular calcification
--Rheumatic heart disease
--Senile calcific stenosis
A

–Mitral annular calcification – large accumulation of Ca in mitral ring impinges conduction system –> arrhythmogenic or providing focus for infective endocarditis and thrombus formation

–Is an incidental finding on CXR, echo, or autopsy

–Carcinoid = endocardial and valvular collagenous thickening

81
Q 
77 y/o woman had episodes of syncope w/ exertion for past month. Afebrile, P66, RR14, 125/85, systolic ejection murmur, few crackles over lung bases posteriorly. Gross appearance of aorta shows calcification. 
What contributed to development of this lesion?
--Aging
--Atherosclerosis
--Chromosomal aneuploidy
--Hypercalcemia of malignancy
--SLE
--Tertiary syphilis
A

–Aging – degenerative change in normal aortic valve w/ aging, appear by age 70-80 –> aortic stenosis

82
Q 
65 y/o woman has health check with only finding being midsystolic click. Within 5 years, she has increasing dyspnea. Echo: mitral regurgitation from prolapse of leaflet. 
What pathologic changes most likely?
--Destructive vegetations
--Dystrophic calcification
--Fibrinoid necrosis
--Myxomatous degeneration
--Rheumatic fibrosis
A

–Myxomatous degeneration –

–Primary from a connective tissue disorder (Marfan) or secondary to chronic hemodynamic forces

–Vegetations = over days to weeks

83
Q 
35 y/o woman has palpitations, fatigue, worsening chest pain for past year. Afebrile, P75, RR 15, 110/70, mid-systolic click w/ late systolic murmur. ROS: 1-2 anxiety attacks/month. 
Echo is likely to show what?
--Aortic valve vegetations
--Mitral valve prolapse
--PDA
--Pulm stenosis
--Tricuspid valve regurgitation
A

– Mitral valve prolapse – symptoms = fatigue, chest pain, arrhythmias; some cases linked to clinical depression and anxiety, others linked to Marfans

  • -Floppy (prolapsed) valve usually asymptomatic
  • -Classic mid-systolic click
84
Q 
11 y/o boy had sore throat, no cough, tonsilar exudates, 38.3C fever 3 weeks ago from culture of group A B-hemolytic Strep. Now: afebrile, P85, RR18, 90/50, diastolic mitral murmur, diffuse rales over both lungs. Next 2 days: several episodes of A-Fib w/ signs of acute LV failure. 
What pathologic changes caused LV failure?
--Amyloidosis
--Fibrinous pericarditis
--Mitral valve fibrosis
--Myocarditis
--Tamponade
--Verrucous endocarditis
A

–Myocarditis – Rheumatic fever complication of acute left ventricular failure = pancarditis (pericarditis, endocarditis, myocarditis)

–myocarditis –> dilation –> incompetent mitral valve

85
Q

14 y/o girl has fever and chest pain for 2wk after a mild URI. T37, P90, RR20, 85/45, friction rub audible. CXR: pulm edema. Echo: small vegetations at closure line of mitral and aortic valves. Endomyocardial biopsy: focal interstitial aggregates of mononuclear cells enclosing areas of fibrinoid necrosis. Improves over next month. Gross appearance of mitral valve shows shortening and thickening of chordae tenidnae and small verrucous vegetations
What cardiac abnormality most likely to occur?
–Constrictive pericarditis
–Dilated cardiomyopathy
–LV aneurysm
–Myxoma
–Valvular stenosis

A

–Valvular stenosis – vegetations cause stenosis of mitral and aortic valves

86
Q

10 y/o girl deevelops subcutaneous nodules over skin of arms and torso 3wks after a bout of acute pharyngitis. Has choreiform movements, pain in knees and hips, particularly on movement, friction rub.
What abnormal serum lab findings is most characteristic of her disease?
–Antistreptolysin O antibody titer
–ANA titer
–Creatinine
–Rapid plasma Reagin (RPR) test
–Troponin I level

A

–Antistreoptolysin O antibody titer – Rheumatic fever = increased: antihyaluronidase, anti-DNase, anti-streptolysin O (ASO) titers

–ANA = SLE –> serous pericarditis

87
Q

25 y/o man found dead at home after not going to work for 3 days. Had splinter hemorrhages under fingernails, no signs of trauma and a large destructive vegetation on aortic valve.
What lab finding is likely to provide evidence of cause of death?
–Elevated anti-streptolysin O titer
–Positive ANCA
–Increased CK-MB fraction
–High dsDNA autoantibody titer
–Positive blood culture for S. aureus

A

–Positive blood culture for S. aureus – infective endocarditis = destructive vegetations that perforate leaflet

  • -Rheumatic fever = verrucous vegetations are small and nondestructive
  • -dsDNA antibody = SLE = Libman-Sacks = nondestructive
88
Q 
22 y/o man develops fever 4 days after tooth extraction. T37.6, high-pitched systolic murmur. Tentative congenital heart disease diagnosis made. 
Where is the congenital anomaly?
--Ascending aorta
--Atrial appendage
--Corda tendinae
--Cusps of valves
--Muscular septum
A

–Muscular septum – small VSD –> L–>R shunt –> systolic murmur (high pitched = small) –> risk for endocarditis

–Most VSD in membranous septum, 10% in muscular septum

89
Q 
26 y/o woman has fever for 5 days. T38.2, P100, RR19, 90/60, murmur heard, sensorium clouded, no focal neurologic deficits. Hb13.1, Plt 233.3k, WBC 19.2k, culture positive for gram (+) bacteria, hematuria. Echo: 1.5cm vegetation on mitral valve.
What is the patient likely to develop?
--Cerebral artery mycotic aneurysm
--Dilated cardiomyopathy
--Myxomatous mitral valve degeneration
--Pericardial effusion w/ tamponade
--Pulmonary abscess
A

–Cerebral arterial mycotic aneurysm – Infective endocarditis of mitral valve –> bacterial septicemia –> septic emboli to systemic circulation –> abscesses

–pulm abscess from right-sided infective endocarditis

90
Q 
19 y/o man has low grade fever for 3 weeks. 38.3C, P104, RR28, 95/60, tender spleen tip palpable, splinter hemorrhages, tender hemorrhagic nodules on palms and soles, heart murmur heard. 
What is infectious agent?
--Coxsackievirus B
--Mycobacterium tuberculosis
--Pseudomonas auruginosa
--Viridans streptococci
--Trypanosoma cruzi
A

–Viridans streptococci – infective endocarditis = prolonged fever, heart murmur, mild splenomegaly, splinter hemorrhages

–Less virulant organism (viridans) = time course of weeks

  • -Pseudomonas = acute bacterial endocarditis over days
  • -Coxsackievirus B and Trypanosoma cruzi = myocarditis
  • -TB = pericarditis
91
Q 
71 y/o woman  has 10kg weight loss, severe nausea and vomiting of blood for 8 months. Afebrile, Hb 8.4, Plt 227k, WBC 6180. Upper GI biopsy: stomach adenocarcinoma. CT abdomen: multiple hepatic masses. Head CT: cystic area in right frontal lobe. 2wk later: severe dyspnea. Chest CT: decreased pulm arterial attenuation
What cardiac lesion likely?
--Calcific aortic valvular stenosis
--Constrictive pericarditis
--Epicardial metastatic carcinoma
--Left ventricular mural thrombosis
--Nonbacterial thrombotic endocarditis
A

–Nonbacterial thrombotic endocarditis – Trousseau syndrome = paraneoplastic marantic vegetations = occur on any cardiac valve, tend to be small, occur w/ hypercoagulable state accompanying malignancies (esp. mucin-secreting adenocarcinomas).

92
Q 
41 y/o woman has increasing dyspnea for 1wk. T37.3, P85, RR20, 150/95, dullness to percussion at lung bases. CXR: bilat pleural effusions, normal heart size. Creatinine 3.1, BUN 29, troponin I 0.1, WBC 3760, Hb 11.7, positive ANA and anti-dsDNA
What cardiac lesions is likely present?
--Calcific aortic stenosis
--Hemorrhagic pericarditis
--Nonbacterial thrombotic endocarditis
--Libman-Sacks endocarditis
--Mural thrombosis
--Rheumatic verrucous endocarditis
A

–Libman-Sacks endocarditis – SLE associated small vegetations that are unlikely to embolize

–SLE = common pericardial effusions, pleural effusions and ascites from serositis

93
Q 
44 y/o woman w/ rheumatic heart disease w/ aortic stenosis has bioprosthetic valve replacement. Stable for 8 years, then develops diminished exercise tolerance
What complication has likely occurred?
--Embolization
--Hemolysis
--MI
--Paravalvular leak
--Stenosis
A

–Stenosis – bioprostheses subject to wear and tear = calcify –> stenosis OR perforate/tear –> insufficiency

–Paravalvular leak = rare early postoperative complication

94
Q 
50 y/o man w/ Hx of infective endocarditis has increasing fatigue and receives bileaflet tilting disc mechanical mitral valve prosthesis. 
What drug should he receive post-surgery?
--Aspirin
--Ciprofloxacin
--Cyclosporine
--Digoxin
--Propranolol
--Warfarin
A

–Warfarin – anticoagulanttherapy necessary for mechanical prostheses to prevent thrombotic complications

–Cant take anticoagulants –> use bioprosthesis (porcine)

95
Q 
44 y/o man has worsened exercise tolerance, marked SOB for 6months. Normal vitals, diffuse rales in all lung fields, pitting edema to knees, Na 130, K 4, Cl 102, CO2 25, creatinine 2, glucose 120. In 100mL of urine: 1.3mmol Na, 40mg creatinine. CXR: cardiomegaly, pulm edema w/ pleural effusions. Echo: 4 chamber cardiac enlargement w/ mitral and tricuspid regurgitation, EF30%. Coronary angio: less than 10% stenosis of coronaries.
What is the diagnosis?
--Amyloidosis
--Hypercholesterolemia
--Familial cardiomyopathy
--Rheumatic heart disease
--Trypanosoma cruzi infection
A

–Familial cardiomyopathy – CHF w/ 4 chamber dilation is suggestive of dilated cardiomyopathy

–FENa is less than 1% = prerenal azotemia

–Amyloidosis = restrictive cardiomyopathy

96
Q 
-- 56 y/o man has increased fatigue, decreased exercise tlerane for 2 years. T37, P75, RR17, 115/75, diffuse crackles, distended abdom w/ fluid wave, bilat pitting edema to knees. CXR: pulm edema, pleural effusions, marked cardiomegaly. Echo: mild tricuspid and mitral regurgitation, reduced RV and LV wall motion, EF30%. Experiences cerebral, renal, and splenic infarctions over the next year.
Chronic use of what produced these symptoms?
--Acetaminophen
--Cocaine
--Ethanol
--Lisinopril
--Nicotine
--Propranolol
A

–Ethanol – symptoms of dilated cardiomyopathy w/ R and L sided heart failure – most common cause is alcohol

97
Q 
25 y/o man suffers sudden cardiac arrest and is resuscitated. Exam: normal vitals. Echo: LV normal, but thinning w/ dilation of RV. Chest MRI: extensive fibrofatty replacement of myocardium w/ no inflammation.
What is most likely cause?
--Cardiomyopathy
--Chagas disease
--HTN
--Long QT syndrome
--Radiation therapy
A

–Cardiomyopathy – arrhythmogenic RV cardiomyopathy = autosomal dominant inherited condition w/ abnormal desmosomal adhesion proteins in myocytes

–Chagas = infection, so has inflammation

98
Q

10 y/o girl has chronic progressive exercise intolerance. T37.1, P70, RR 14, 100/60. CXR: cardiomegaly, mild pulm edema. Echo: severe LVH, prominent intraventricular septum, RV slightly thickened, mitral anterior leaflet moves into LV outflow tract during systole, abnormally high EF, low ventricular volume, low CO.
What is the likely cause if cardiac abnormalities?
–Autoimmunity against myocardial fibers
–B-myosin heavy chain gene mutation
–Deposition of amyloid fibrils
–Excessive iron accumulation
–Latent enterovirus infection

A

– B-myosin heavy chain mutation – Hypertrophic cardiomyopathy = familial in 70%+ of cases, autosomal dominant = mutation in proteins of cardiac contractile elements

99
Q

17 y/o girl jumps playing v-ball and suddenly collapses and requires cardiopulmonary resuscitation. Happens again a month later. Has been healthy and complained only of limited chest pain episodes during v-ball this school year.
What pathologic findings is likely?
–Extensive myocardial hemosiderin deposition
–Haphazardly arranged hypertrophied septal myocytes
–Large, friable vegetations w/ destruction of aortic valve cusps
–Mitral valvular stenosis w/ L atrial enlargement
–Tachyzoites within foci of myocardial necrosis and inflammation

A

–Haphazardly arranged hypertrophied septal myocytes – hypertrophic cardiomyopathy = most common cause of sudden unexplained death in young athletes = asymmetric septal hypertrophy –> reduces EF of LV, esp. during exercise

  • -Hemochromatosis = middle aged cardiomyopathy
  • -Tachyzoites = Toxoplasmosis gondii –> myocarditis
100
Q

86 y/o man has increasing dyspnea and reduced exercise tolerance for 7yrs. Afebrile, 135/85, irregular heartbeat averaging 76, crackles at base of lungs. CXR: mild caridomegaly, mild pulm edema. Echo: slight RV and LV wall thickening w/ reduced wall motion, reduced LV filling, EF25%. Endomyocardial biopsy: amorphous pink-staining depostis between myocardial fibers, no inflammation or necrosis.
Echo would likely show what functional disturbance?
–Dynamic obstruction of ventricular outflow
–Impaired ventricular diastolic filling
–Increased end-systolic volume
–Mitral and tricuspid insufficiency
–reduced EF

A

–Impaired ventricular diastolic filling – Cardiac sarcoidosis –> myocardial fiber dysfunction –> restrictive cardiomyopathy = reduced chamber compliance

101
Q 
33 y/o woman from Victoria, BC has increasingly severe dyspnea, orthopnea, and leg swelling for 2 weeks. No Hx of  serious illness or surgery. T37.8, P83, RR20, 100/60. ECG: V-tachycardia. Echo: RV and LV dilation, no valve deformities. Endomyocardial biopsy: focal myocyte necrosis, lymphocyte infiltrate
Infection by what organism?
--Coxsackievirus A
--Mycobacterium kansaii
--Viridans streptococci
--S. aureus
--Toxoplasma gondii
--Trypanosoma cruzii
A

–Coxsackievirus A – viral myocarditis = focal myocardial necrosis w/ lymphocytic infiltrate

–In North America, most cases caused by Coxsackievirus A and B

–Viridans and S. aureus = neutrophilic infiltrate

102
Q 
68 y/o man becomes increasingly lethargic and weak for past 7months. T36.9, P70, RR15, 160/105, friction rub audible. Gross appearance of epicardium is rough, corrugated brown color, "bread and butter" appearance. 
What lab findings?
--Elevated ASO titer
--Elevated Renin
--Increased BUN
--Increased CK-MB
--Positive ANA w/ "rim" pattern
--Positive viral serology
A

–Increased BUN – Fibrinous pericarditis most common cause is uremia resulting in renal failure

103
Q 
52 y/o woman has chronic cough w/ occasional blood-streaked, whitish sputum for 2yrs. T37.9, P72, RR22, 125/80, crackles over upper lung fields, faint heart sounds, 15mmHg inspiratory decline in systolic arterial pressure. CXR: prominent heart borders w/ "water bottle" configuration. Pericardiocentesis: 200mL of bloody fluid.
What organism produced this?
--Candida albicans
--Coxsackievirus B
--Group A strep
--Mycobacterium tuberculosis
--S. aureus
A

–Mycobacterium tuberculosis – hemorrhagic pericarditis most common cause are: metastatic carcinoma, TB

  • -Cardiac tamponade –> low CO
  • -Pulsus paradoxus = drop in pressure in inspiration
104
Q

31 y/o man has chest pain, increasing dyspnea, nausea, and loss of consciousness multiple times. Dies 7 days later in sleep. No evidence of trauma. He was 5ft5in, 75kg (BMI 27). Gross appearance of chest cavity shows massive hemopericardium w/ pericardial tamponade.
What was underlying cause?

A

–Coronary atherosclerosis – MI –> Transmural MI rupture 3-7 days later

105
Q

73 y/o woman has episodes of chest pain for past week. Afebrile, P80, RR16, 110/70, distant heart sounds, clear lung fields, JVD to angle of jaw even when sitting, darkly pigmented, irregular 1.2cm lesion on right shoulder. CXR: prominent L and R heart borders. Pericardiocentesis: bloody fluid. Lab: troponin I 0.3.
What lesion most likely caused this findings?
–Calcific aortic stenosis
–Coronary atherosclerosis
–Epicardial metastases
–Mitral valvulitis
–Tuberculous pericarditis

A

–Epicardial metastases – Most common neoplasm involving heart is metastatic cancer (commonly from nearby lung, breast and esophagus), in this case melanoma

106
Q 
48 y/o woman suddenly loses consciousness 4x in past 6 months. 3 instances for few minutes, 4th episode 1 month ago was unconscious for 6 hours and had weakness in her right arm and difficulty speaking. Afebrile, normal BP, no murmurs, good carotid pulses w/o bruits. 
What cardiac lesion most likely present?
--Bicuspid aortic valve
--Coronary artery thrombosis
--Left atrial myxoma
--Mitral valve stenosis
--Pericardial effusion
A

–Left atrial myxoma – most common primary cardiac neoplasm = produce ball-valve effect –> intermittently occlude mitral valve –> syncopal episodes, possible stroke from embolization

107
Q

55 y/o man undergoes orthotopic cardiac transplant. 2mo later, endomyocardial biopsy shows focal myocardial cell death w/ scattered perivascular lymphocytes and plasma cells. Treated w/ sirolimus (macrolide immunosuppressant)
What pathologic process accounts for this?
–Autoimmunity
–Autophagy
–Ischemia
–Infection
–Rejection

A

–Rejection – acute cellular rejection amenable to therapy w/ immunosuppression.

108
Q

45 y/o man receives cardiac allograph for dilated cardiomyopathy. No rejection problems, but 5yrs later has worsening exercise tolerance w/ increasing dyspnea and peripheral edema. Echo: EF35%
What pathologic abnormalities developed in allograph?
–Amyloidosis
–Constrictive pericarditis
–Coronary arteriopathy
–Non-Hodgkin lymphoma
–Toxolasmosis

A

–Coronary arteriopathy – nearly every every allograft develops some degree of arteriopathy within 10 years –> ischemic damage –> symptoms

109
Q 
24 y/o primigravida has fetal ultrasound at 18wks: normal amniotic fluid index, large echogenic region in right lung. Soon after delivery, term infant has resp distress. CT: normal left lung, opacification area in right lung supplied by a vessel from the aorta.
Diagnosis?
--Extralobar sequestration
--Foregut cyst
--Hyaline membrane disease
--Oligohydraminos sequence
--Tracheoesophageal fistual
A

–Extralobar sequestration – produces external mass effect on normal lung, limits gas exchange b/c not connected to airway, has anomalous systemic arterial connection

  • -Intralobar sequestration = in lung parenchyma, recurrent infections in childhood
  • -Foregut cysts = in hilum or mediastium, not on connected to airways, large = mass effect
110
Q

30 y/o man hospitalized after MVA w/ blunt trauma to chest. Exam: contusion on R chest, no lacerations. 1hr after: suddent difficulty breathing, marked pain on right side. Afebrile P80, RR30 and shallow, 100/65, not audible breath sounds, tympany to percussion on R side.
What radiologic finding?

A

–Pneumothorax – blunt trauma –> rib fracture –> sharp bone penetrate pleura –> air leak –> pneumothorax

111
Q

58 y/o man w/ ischemic heart disease has CABG under general anesthesia. 2day postop: increasing resp difficulty w/ decreasing PaO2. P78, RR25, 135/85, Hb 13.7 unchanged since surgery. After he coughs up large amount of mucoid sputum, condition improves.
What kind of atelectasis (alveoli collapse)?

A

–Resorption atelectasis – result of mucous or mucopurulent plug obstructing bronchus –> air in alveoli distal to obstruction is resorbed –> collapse of that part of lung

  • -Compression atelectasis = from accumulation of fluid or air in pleura = same as relaxation atelectasis
  • -Contraction atelectasis = fibrous tissue surrounds lung
  • -Microatelectasis = post-op, diffuse alveolar damage or newborn loss of surfactant
112
Q

45 y/o 45 y/o man incurs blunt chest trauma. Exam: R chest wall pain. CXR: fractured R 7th rib. Next 2 days: subcutaneous tissue swelling w/ non-painful crepitance on palpation.
Leakage of what is likely to produce swelling?

A

–Air – trauma –> air leak w/ interstitial emphysema

113
Q 
68 y/o man has worsening dyspnea and orthopnea w/ increased frothy sputum for 3 yrs. Crackles at lung bases. CXR: bilat interstitial infiltrate, distinct Kerley B lines, prominent L heart border. Na 135, K 3.8, Cl 99, CO2 25, glucose 76, creatinine 1.5, BUN 30, FENa less than 1%. Renin, Aldosterone, ADH, BNP (natriuretic peptide) all increased.
What pathologic finding most likely?
--Aldosteroma
--Bilateral adrenal atrophy
--Chronic glomerulonephritis
--Ischemic heart disease
--Pulmonary fibrosis
--Small cell carcinoma
A

–Ischemic heart disease – L heart failure w/ pulmonary edema and congestion = reduced CO –> diminished renal blood flow –> RAAS –> increased plasma volume –> pulmonary edema

–Characteristic prominent L heart border

114
Q 
26 y/o woman w/ postpartum sepsis is afebril on abx therapy, but worsening O2 sat for past 3days. CXR: scattered bilat pulm opacifications. Ventilation-perfusion scan shows mismatch. 
What microscopic findings?
--Alveolar hyaline membranes
--Arterial plexiform lesions
--Insterstitial fibrosis
--Lymphocytic infiltrates
--Respiratory bronchiolar destruction
A

–Alveolar hyaline membranes – acute lung injury w/ noncardiogenic pulm edema and development of diffuse alvolar damage (DAD) = ARDS

  • -Plexiform lesions = characteristic of pulmHTN
  • -Lymphocytes = viral or immune-mediated disease
  • -Bronchiolar destruction = centrilobar emphysema
115
Q

After hemicolectomy for colon carcinoma, 56 y/o man develops resp distress. Intubated, mechanichal vent w/ 100%O2. 3days later: PaO2 decreases to 60%. CXR: increasing opacification in all lung fields. Transbronchial lung biopsy histo: hyaline membranes lining distended alveolar ducts and sacs
What mechanism?
–Aspiration of oropharyngeal contents
–Intravascular thrombi w/ coagulopathy
–Leukocyte-mediated injury to alveolar capillaries
–Reduced production of surfactant
–Release of fibrogenic cytokines by macrophages

A

–Leukocyte mediated injury to alveolar capillaries – clinical and morphologic presentation of acute lung injury –> severe form is ARDS = characterized by DAD caused by injury to capillary endothelium w/ neutrophils and macrophages

  • -Fibrogenic cytokines = chronic diffuse pulm fibrosis
  • -Reduced surfactant = newborn resp distress syndrome
116
Q

48 y.o man has gradually increasing dyspnea and 4kg weight loss in past 2yrs. Smoked 2pk/day for 20yrs, but not past year. Increased anterioposterior diameter of chest, decreased breath sounds. CXR: bilat hyperlucent lungs, esp. in upper lobes. Pulm fxn test: markedly decreased FEV1, normal FVC, decreased ratio.
What contributed to pathogenesis of his disease?
–Abnormal epithelial cell Cl ion transport
–Decreased ciliary motility w/ irregular dynein arms
–Impaired hepatic release of a1-antitrypsin deficiency
–Macrophage recruitment and release of IFN-gamma
–Release of elastase from neutrophils

A

–Release of elastase from neutrophils – COPD w/ centrilobar pattern = subtle long term inflammation –> neutrophil and macrophage elaboration of elastase not inhibited by A1AT –> loss of lung tissue

  • -IFN-gamma = from T-cells, typical of chornic inflammation and pneumoconioses
  • -Dynein arms = Kartagener syndrome –> bonchiectasis
  • -Cl transport = Cystic Fibrosis –> bronchiectasis
117
Q 
20 y/o falls to ground when jogging one morning, suddenly becomes markedly SOB. No breath sounds audible over right side. CXR: shift of mediastinum from R to L. Chest tube inserted on R side and air rushes out.
What underlying disease?
--Asthma
--Bronchiectasis
--Centriacinar emphysema
--Chronic bronchitis
--Distal acinar emphysema
--Panlobular emphysema
A

–Distal acinar emphysema – Distal acinar (paraseptal) emphysema = localized, beneath pleural, typically upper lobe, prone to rupture –> pneumothorax

–Cause of spontaneous pneumothorax in young adults

  • -Centriacinar = smokers
  • -Panacinar (panlobular) = A1AT deficiency common cause
118
Q 
49 yo man has increasing dyspnea for 4yrs, occasional cough w/ minimal sputum. Lungs hyperresonant w/ expiratory wheezes. Pul fxn tests: increased TLC, slightly increased FVC, decreased FEV, decreased ratio. ABG: pH 7.35, PO2 65, PCO2 50. 
What disease process?
--Centrilobar emphysema
--Chronic pulmonary embolism
--Diffuse alveolar damage
--Nonatopic asthma
--Sarcoidosis
--Silicosis
A

–Centrilobar emphysema – findings point to obstructive lung disease = airway narrowing and loss of recoil = emphysema

119
Q 
33 y/o man has increasing dyspnea for 8yrs, doesn't smoke. Decreased breath sounds over lower lung fields. CzXR: flattened diaphragms. Pulm fxn test: decreased DLCO, FEV1, increased FVC, decreased ratio. ABG: PO2 65, PCO2 60, HCO3 32, pH 7.35. Sibling is also affected
What mechanism of his pulm disease?
--Atopy w/ IgE binding to mast cells
--CFTR gene mutation
--Increased neutrophil proteases
--Prior infection w/ TB
--Reduced antielastase activity
A

–Reduced antielastase activity –emphysema = increased lucency in all lung fields and increased anterior-posterior diameter

DLCO = diffusion of lung CO to blood – demonstrates gas uptake ability

120
Q

45 y/o man smoked 2pk/day for 20yrs had chronic cough w/ copious mucoid expectoration for past 4yrs. Past yr: multiple resp tract infections diagnosed as viral flu, developed difficulty breathing, thightness of chest, audible wheezing. Breathing difficulty relieved by B-agonist, disappears after chest infection resolved.
What condition is responsible for his condition?

A

–Chronic asthmatic bronchitis – chronic bronchitis diagnosis made clinically (persistent cough w/ sputum for 3 months in 2 consecutive years) = disease of smokers, poor air quality

121
Q

In study of smokers (1pk+/day for 30yrs), pulm fxn test shows subset w/: decreased FEV1, normal to decreased FVC, decreased FEV1/FVC ratio below 70%.
What resp tract structure is likely affected by underlying disease in this subset?

A

–Respiratory bronchiole – centilobar emphysema = damage to central part of lung acinus = dilation of resp bronchioles sparing distal alveolar ducts and alveolar sacs

122
Q

62 y/o smoker w/ 10yr Hx of cough w/ copious mucopurulent sputum has progressive dyspnea for 6months. Bilat pedal edema, soft but enlarged liver. CXR: bilat pleural effusion, prominent R heart border. ABG: PO2 60, PCO2 52, pH 7.3, HCO3 29. Intubated, on ventilator requiring increasing O2.
What microscopic finding?
–Bronchovascular distribution of granulomas
–Carcinoma filling lymphatic spaces
–Extensive interstitial fibrosis
–Hypertrophy of bronchial submucosal glands
–Mucosal infiltrates of eosinophils

A

–Hypertrophy of bronchial submucosal glands – Chronic bronchitis can lead to pulmHTN and cor pulmonale

–Granulomas = sarcoidosis or mycobacteria

123
Q

12 y/o girl has 7yr Hx of coughing, wheezing, repeated attacks of difficulty breathing (common in Spring). During episode: lungs hyperresonant on percussion, CXR: increased lucency of all lung fields, increased IgE, eosinophilia.
What histological feature likely?
–Dilation of resp bronchioles w/ loss of elastic fibers
–Inflammatory destruction of bronchial walls
–Interstitial and alveolar edema w/ hyaline membrane formation
–Pathy areas of consolidation w/ leukocytic exudates in alveoli
–Remodeling of airways w/ smooth muscle hyperplasia

A

–Remodeling of airways w/ smooth muscle hyperplasia – atopic asthma –> episodes of inflammation –> remodeling and SmM hyperplasia

124
Q

33 y/o man has sudden dyspnea and wheezing, RR35, CXR: increased lucency of all lung fields, PO2 65, PCO2 30, pH 7.48, Curschmann spirals, Charcot-Leyden crystals, branching septate hyphae, and eosinophilia in abundant mucus on sputum cytology.
What risk factor predisposes him to this?
–Cytokine gene polymorphisms
–Foreign body aspiration
–Inhalation of environmental inorganic dusts
–Inheritance of a CFTR gene mutation
–Reduced circulating A1AT
–Cigarrete smoking for 10+ years

A

–Cytokine gene polymorphisms – atopic (extrinsic) asthma is type 1 hypersensitivity associated w/ excessive Th2 and Th17 cell-mediated immune response, linked to cytokine genes on 5q

  • -Curschmann spirals = whorls of sloughed surface epithelium
  • -Charcot-Leyden crystals = breakdown products of eosinophil granules
125
Q

Inhaled drug reducing which mediator is most likely to be effective treating recurrent bronchial asthma?

  • -Th1 cytokines
  • -Vasoactive amines
  • -Th2 cytokines
  • -Leukotrienes
  • -Prostaglandins
A

–Th2 cytokines

126
Q

35 y/o man has 5yr Hx of episodic wheezing and coughing, more common in winter, often followed by minor resp tract infections, no family Hx of asthma, normal Ige and WBC
What mechanism contributes to his illness?
–Accumulation of alveolar neutrophilic exudate
–Bronchial hyperreactivity to chronic inflammation
–Emigration of eosinophils to bronchi
–Hyperresponsiveness to Aspergillus spores
–Secretion of IL4 and IL5 by T cells

A

–Bronchial hyperreactivity to chronic inflammation – nonatopic, intrinsic, asthma = bronchial hyperresponsiveness (triggered by pollutants, ozone, sulfer dioxide, nitrogen diozide, exercise, cold air)

127
Q 
Study of atopic asthma reveals smooth muscle change and mucus gland hypertrophy.
What immune cells are most important in excessive response to allergens?
--B lymphocytes
--Cytotoxic lymphocytes
--NK cell
--Th1 lymphocyte
--Th2 lymphocyte
--Th17 lymphocyte
A

–Th2 lymphocyte – drives cytokine production (IL4, IL5, IL13) –> eosinophilic infiltration, IgE production by mast cells

  • -Th1 = granulomatous inflammation
  • -Th 17 = inflammation to infectious agents, autoimmunity?
128
Q 
70 y/o woman has episodes of dyspnea, wheezing, coughing, and urticaria for 3yrs. Also had bouts of rhinitis. 10yr Hx of osteoarthritis. Exam: nasal polyps
What drug caused her resp disease?
--Acetaminophen
--Aspirin
--Gabapentin
--Morphine
--Prednisone
A

–Aspirin – Drug-induced asthma = old person develops asthma

–ACE inhibitors can also produce asthma-like episodes

129
Q

19 y/o man w/ recurrent mucoid rhinorrhea w/ chronic sinusitis and otitis media since childhood and multiple bouts of pneumonia. Tactile fremitus, ronchi, rales in lower lung fields, nasal polyps. CXR: bronchial dilation w/ wall thickening, focal atelectasis, areas of hyperinflation, heart shadow on right.
What is it?

A

–Kartagener syndrome (sinusitis, bronchiectasis, situs inversus w/ ciliary dyskinesia) = abnormal ciliary dynein arms

130
Q

35 y/o woman w/ multiple bouts of necrotizing pneumonia since childhood has H. influenzae, S. aureus, Pseudomonas aeruginosa, Serratia marcescens cultured from sputum. Has cough w/ purulent sputum, dullness to percussion, decreased breath sounds. CXR: R lower lobe consolidation. Bronchogram shows dilation of right lower lobe bronchi
What disease mechanism?
–Congential malformation of bronchial walls
–Damage to bronchial mucosa by major basic protein of eosinophils
–Diffuse infiltration by bronchogenic carcinoma
–Recurrent inflammation w/ bronchial wall destruction
–Unopposed action of neutrophil-derived elastase on bronchi

A

–Recurrent inflammation w/ bronchial wall destruction – Bronchiectasis = prolonged infections or obstruction –> irreversible dilation of bronchi –> chronic obstructive airway disease

–Unopposed elastase = emphysema

131
Q

Polymorphisms in what gene can lead to some heavy smokers having less parenchymal destruction with centrilobar emphysema than other heavy smokers?

  • -A1AT
  • -BMPR2
  • -CFTR
  • -GM-CSF
  • -TGF-B
A

–TGF-B – cytokine involved in mesenchymal cell response to lung injury

132
Q 
63 y/o man has progressively worsening dyspnea for 10 years and 5kg weight loss for past 2yrs. Chronic cough w/ minimal sputum, no chest pain, afebrile, normotensive, CXR shows extensive interstitial disease. Pulm fxn test: diminished DLCO, low FVC, normal ratio. 
Increased exposure to what caused this?
--CO
--Ozone
--Silica
--Tobacco smoke
--Wood dust
A

–Silica –crystals incite fibrogenic response after inhalation and ingestion by pulm macrophages

133
Q

Study of miners with exposure to inhaled dust of 1-5micron particles that are inert and insoluble that cause fibrosis. What is it?

A

–Carbon – Coal worker’s pneumoconiosis is w/ carbon

134
Q

76 y/o man has dyspnea for 4yrs. CXR: increased interstitial markings, no effusions, prominent R heart border and pulm arteries. Biopsy stained w/ Prussian blue show ferruginous bodies
What inhaled substance?

A

–Asbestos –ferruginous bodies = long, thin crystals of asbestos encrusted w/ iron and calcium

135
Q

One pattern of inhalation lung disease: decreased lung capacity, diffusing capacity, and compliance, numerous bilatral nodular opacifications on CXR, polarizable needlelike crystals.
What inhaled substance?

A

–Silica dust – silicotic nodules

136
Q

ABG: pH7.45, PO2 83, PCO2 30, HCO3 19
Pulm fxn: low total lung capacity, FEV1, DLCO, pulm compliance
What restrictive disease?

A

–Sarcoidosis – hilar adenopathy, reticulonodular infiltrates characteristic of sarcoid

137
Q

65 y/o man who worked installing fire retardant insullation has progressive dyspnea, resp failure, and hypoxemia. CT: large mass encasing left lung
What finding on CXR?
–Bilateral fluffy perihalar infiltrates
–Bilateral upper lobe cavitation
–Diaphragmatic pleural calcified plaques
–Endobronchial mass w/ atelectasis
–Pleural effusions

A

–Diaphragmatic pleural calcified plaques – Asbestosis = common pleural fibrosis and interstitial lung disease seen as dense pleural plaque, often calcified

–Mass = mesothelioma

138
Q

64 y/o alfalfa farmer has 15yr Hx of increasing dyspnea. CXR: bilat increased linear markings. Reduced FVC, normal FEV1. Interstitial infiltrates of lymphocytes and plasma cells, minimal interstitial fibrosis, small granulomas.
What is it?

A

–Farmer’s lung = hypersensitivity pneumonitis caused by inhalation of actinomycete spores in moldy hay – type 3 (early) and type 4 (chronic) immune hypersensitivity

139
Q

25 y/o man moves to new apartment and has fever, cough, dyspnea, headache, and malaise. Leaves for 3 days and symptoms subside. Comes back and symptoms recur.
What is it/

A

Hypersensitivy pnemonitis – antigen-antibody complex-mediated injury

–often from actinomycetes or fungi (molds) growing in contaminated HVAC

140
Q

46 y/o man w/ increasing dyspnea, nonproductive cough: afebrile, clubbed digits, mild restrictive abnormality, reduced DLCO, numerous alveolar macrophages (with lamellar bodies and iron pigment inside), plump epithelial cells, mild interstitial fibrosis, loss of resp bronchioles.
What is it? What caused it?

A

–Desquamative interstitial pneumonitis – smoking-related interstitial lung disease

–treat w/ smoking cessation and corticosteroid

141
Q

68 y/o woman has a saddle embolism and dies.

What mechanism for sudden death?

A

–Acute cor pulmonale – pulmonary HTN causing R heart failure

–Also could be hypoxemia?

142
Q

45 y/o man has progressive dyspnea, prominent pulmonary component of S2, systolic murmur of tricuspid insufficiency, bruit over peripheral lung fields, JVD to angle of jaw, (+) antiphospholipid Ab, eccentric occlusions w/ pulm arteries and mosaic attenuation of pulm parenchyma.
What lung disease?

A

–Thromboembolism – multiple small PE –> reduce vascular bed –> recanalization –> narrow channels –> bruits –> pulm HTN –> cor pulmonale

–Antiphospholipid antibodies = thrombosis risk

143
Q

Patient w/ large ASD develops pulmHTN –> cor pulmonale –> shunt direction change
What is this called?

A

–Eisenmenger complex – R–>L shunt reverses due to increase R atrial pressure

144
Q

25 y/o woman w/ primary pulmonary HTN likely has a mutation in what gene

  • -B-type natriuretic peptide (BNP)
  • -Bone morphogenetic receptor 2 (BMPR2)
  • -Endothelial nitric oxide synthetase (eNOS)
  • -Fibrillin-1
  • -Lysyl hydroxylase
  • -Renin
A

–Bone morphogenetic receptor 2 (BMPR2) – cell surface protein TGF-B receptor superfamily – inactivation mutation

–Lysyl hydroxylase = Ehlers-danlos syndrome

145
Q

29 y/o man has acute onset hemoptysis, 150/95, bilat fluffy lung infiltrates, focal necrosis of alveolar walls, intra-alveolar hemorrhage, oliguria, creatinin 2.9, BUN 31.
What antibody?

A

–Anti-glomerular basement membrane antibody – Goodpasture syndrome = affect kidney and lung basement membrane = type 2 hypersensitivity

146
Q

In a study, those who receieved general anesthesia andintubation were more likely to develop pulm infections 2 week later than those who did not intubated or anesthetized.
What is the anesthetic mechanism to increase risk?

A

–Decreased ciliary function – anesthetic gases tend to reduce ciliary function of respiratory epithelium that lines bronchi

147
Q

54 y/o woman has cough w/ yellowish sputum for 4 days, fever, WBC 12k w/ 71% neutrophils, 9% bands.
What organism is likely to be culturedin sputum?

A

–Streptococcus pneumoniae – Pneumococcus most likely for acquired pneumonia outside of the hospital

148
Q

71 y/o woman smoked 1pk/day for 50yrs has fever, productive cough, severe dyspnea for 3days, rales, expiratory wheezes, peripheral blood neutrophilia.
What organism most likely cultured in sputum?
–Histoplasma capsulatum
–Influenza A
–Moraxella catarrhalis
–Mycobacterium kansasii
–Pneumocystitis jiroveci

A

–Moraxella catarrhalis – only organism causing both upper and lower resp infections, esp in COPD patients = gram (-) diplococci, oxidase (+)

  • -Pneumocystitis = immunocompromised pneumonia
  • -M. kansasii = pulm granulomatous disease
149
Q

51 y/o drunkard has fever, crackles, 3cm lesion in w/ air-fluid level in right lower lobe. He has aspiration pneumonia.
What common organisms?

A
  • -Most common = S. aureus

- -Anaerobes = Bacteriodes, Peptococcus, Fusobacterium

150
Q

20 y/o man has mild fever, nonproductive cough, headache, myalgias for 1wk, erythema of pharynx, diffuse crackles, bilat extensive patchy lung infiltrates, normal flora on gram stain, elevated cold agglutinin. Improves from erythromycin.
What organism?

A

–Mycoplasma pneumoniae – primary atypical pneumonia = similar finding to viral infection, but responds to erythromycin

151
Q

Influenza Virus A antigenic type H5N1 causes avian flu, which has 60% mortality. Enhanced pathogenicity is due to mutation that enables it to do what?

  • -Elicit weak cytotoxic T-cell response
  • Enter many types of host cells
  • -Escape inactivation by macrophages
  • -Infect CD4+ helper T cells
  • -Spread from humans to humans
A

–Enter many types of host cells – Hemagglutinin (H) or neuraminidase (N) gene alteration allows them to escape host antibodies.

–Hemagglutinin cleavage by host proteases allows them to enter host cells

152
Q

What 2 viruses, which are indistinguishable clinically, are the most common causes of pediatric lower respiratory infection?

A
  • -Human metapneumovirus

- -Respiratory syncytial virus

153
Q 
HIV infected patient w/ CD4 below 100 has pulmonary infection that causes: hepatosplenomegaly, lymphadenopathy, malabsorption w/ weight loss, night sweats, fever, macrophages filled w/ acid-fast infectious organisms
What organism?
--Aspergillus niger
--Candida albicans
--Legionella pneumophilia
--Mycobacterium avium-complex
--Nocardia asteroides
--Pseudomonas aeruginosa
A

–Mycobacterium avium-complex (MAC) – most likely to become disseminated illness in immunocompromised persons

–acid fast, proliferate in macrophages

154
Q

What WBC differential is found in a patient w/ primary TB infection?

A

–Lymphocytosis and monocytosis

155
Q

46 y/o man from northern Mexica has fever, cough, weight loss, miliary pattern of nodules in all lung fields, 50micron diameter organisms w/ thick walls filled w/ endospores
What organism?

A

–Coccidioides – endemic to semiarid region in Americas

156
Q

56 y/o man undergoing chemotherapy has fever, cough, dyspnea, chest pain, hemoptysis, 1-4cm nodular densities w/ surrounding ground-glass infiltrate (halo sign), narrow branching septate hyphae.
What organism?

A

–Aspergillus fumigatus – invasive aspergillosis in immunocompromised patients w/ neutropenia

157
Q

43 y/o woman w/ HIV has pneumonia. Bronchial fluid stains w/ Gomori methenamine silver stain.
What organism?

A

–Pneumocystis jiroveci– most often associated w/ AIDS and is diagnostic of AIDS in HIV infected patients

158
Q

64 y/o chain-smoker has 5kg weight loss in 3mo, clubbed fingers, no hilar adenopathy, cavitation w/ 3cm lesion in right hilum, Ca 12.3, Phosphorus 2.4, Albumin 3.9, lesion almost occluding right main bronchus.
What neoplasm?

A

–Squamous cell carcinoma – most likely lung cancer to produce paraneoplastic hypercalcemia, has strong association w/ smoking, undergoes central necrosis

159
Q

50 y/o smoking man has 4cm mass in left hilum, cytology of round epithelial cells that have appearance of lymphocytes but larger. Told that although it is localized to one side, surgical treatment is unlikely to be curative and to stop smoking.
What neoplasm?

A

–Small cell anaplastic carinoma – small cell carcinoma –> ectopic corticotrophin production –> paraneoplastic Cushing syndrome

MQW U4 (9 decks)

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