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Tri 4 - Pathology II > Test 2 > Flashcards

Test 2 Flashcards

1
Q

What are the genetic factors of congenital heart dz?

A

trisomies 13, 15, 18, 21, and Turner’s Syndrome (monosomy X)

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2
Q

What is the relative incidence of congenital heart dz?

A
  • ventricular septal defects: 25-30%
  • atrial septal defects: 10-15%
  • patent ductus arteriosus: 10-15%
  • tetralogy of Fallot: 6%
  • pulmonary stenosis: 6%
  • coarctation of the aorta: 6%
  • aortic stenosis: 6%
  • complete transposition of the great arteries: 6%
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3
Q

Which congenital heart dz’s present with a/cyanosis?

A
  • acyanotic: patent ductus arteriosus, atrial septal defect (PFO), ventricular septal defect
  • cyanotic: tetralogy of Fallot, pulmonary stenosis, transposition of great arteries
  • cyanosed tardive: an initial L-to-R shunt with late reversal of flow
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4
Q

What are atrial septal defects?

A
  • primum: adjacent to AV valves, leads to cleft mitral valve defect
  • secundum: fossa ovalis defect, m/c (90%)
  • complications: atrial arrhythmias, pulmonary hypertension, R ventricular hypertrophy, heart failure, thrombo-emboli
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5
Q

What are ventricular septal defects?

A
  • m/c congenital heart defect, often occurring with tetralogy of Fallot
  • NO cyanosis as long as L side pressure is higher than the R
  • increased blood flow to R ventricle results in thickening of pulm aa, increased vascular resistance, and reversal of shunt (Eisenmenger complex) => cyanosis
  • complications: infective endocarditis, paradoxical emboli, aortic valve cusp prolapse
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6
Q

What is patent ductus arteriosus?

A
  • shunting of blood from aorta to pulm aa results in pulmonary hypertension
  • features: mostly asymptomatic but presence of harsh murmur, common with Down syndrome, and in premature infants or those whose mothers were infected with rubella early in pregnancy
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7
Q

What is tetralogy of Fallot?

A
  • m/c cause of cyanotic congenital heart disease
  • cardiac features: pulmonary stenosis, ventricular septal defect, dextro-position of the aorta, R ventricular hypertrophy = boot shape
  • clinical features: cyanosis (Tet spell during crying or feeding), fingertip clubbing
  • complications: cerebral thrombosis, bacterial endocarditis, brain abscesses
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8
Q

What is transposition of great vessels?

A
  • aorta arises from RV, pulmonary trunk from LV
  • almost all infants have ASD, two-thirds have PDA, and half have VSD
  • 90% die in first yr b/c deox blood from RV goes to aorta
  • m/c in males, cause is usually idiopathic, present with cyanosis
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9
Q

What is coarctation of the aorta?

A
  • local constriction that occurs immediately below the origin of the L subclavian a. at the site of the ductus arteriosus
  • m/c in males, or females with turner’s syndrome
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10
Q

What are the clinical features of coarctation of the aorta?

A
  • hypertension in upper part of body
  • L ventricular hypertrophy
  • increased pressure increases risk of Berry aneurysm and subarachnoid hemorrhage
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11
Q

What is stenosis/atresia?

A
  • pulmonary stenosis/atresia: hypoplastic RV with ASD
  • aortic stenosis/atresia: valvular => hypoplastic LV; sub-valvular (subaortic) => aortic thickening below the cusps; supra-valvular => aortic thickening above the cusps
  • complications: Eisenmenger syndrome (cyanotic heart dz)
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12
Q

What are the functions of the endothelial cells of the blood vessels?

A
  • act as a permeability barrier
  • vasoactive factors (NO, endothelin)
  • antithrombotic agent production (PG12)
  • anticoagulant production (thrombomodulin)
  • fibrinolytic agent production (plasminogen)
  • procoagulant production (von Willebrand factor)
  • inflammatory mediator production (IL-1)
  • growth factor production (growth factors)
  • growth inhibition (heparin replication)
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13
Q

What is arteriosclerosis?

A
  • any dz process that hardens arteries
  • atheroma: fibro-inflammatory-lipid plaque accumulating in lrg or med aa. intimal layer
  • complications: ischemic heart dz, MI, stroke, extremity gangrene
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14
Q

How do atherosclerotic plaques form?

A
  • m/c b/c of oxidative stress
  • inflammation increases permeability
    => angiotension 2 receptor increases cell adhesion
    => monocytes infiltrate endothelium and transform into macrophages
    => macrophages accumulate, engulf lipids, and turn into foam cells
    => smooth mm proliferation and deposition of collagen and lipids alters the arterial wall
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15
Q

What is vasculitis?

A
  • inflammation of vessel walls, usually arteries
  • symptoms: fever, malaise, myalgia, arthralgia
  • can be infective d/t neisseria, rickettsia, syphilis, varicella, or hep B
  • can be d/t to immunological injury like serum sickness, autoimmune conditions, Wegener’s granulomatosis, Goodpasture syndrome, or Kawasaki dz
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16
Q

What is polyarteritis nodosa?

A
  • transmural inflammation of the arterial wall
  • necrotizing vasculitis of organs with prominent renal involvement, also fever and weight loss
  • m/c in young adults in the medium-sized vessels
  • morphology: fibrinoid necrosis in affected artery, also present are leukocytes and plasma cells
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17
Q

What is Kawasaki dz?

A
  • acute necrotizing vasculitis of infancy and early childhood
  • symptoms include high fever, rash, conjunctival and oral lesion, lymphadenitis, strawberry tongue
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18
Q

What is Wegener’s granulomatosis?

A
  • systemic necrotizing vasculitis of small vessels
  • m/c in men in the fifth and sixth decades of life
  • presents with granulomatous lesions of the nose, sinuses, and lungs, along with renal glomerular dz, and positive for anti-neutrophil cytoplasmic Ab’s (ANCA)
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19
Q

What is Wegener’s triad?

A
  1. Acute necrotizing granulomas in the respiratory tract, leading to cavitations
  2. Focal necrotizing or granulomatous vasculitis in small to medium-size vessels
  3. Renal dz: crescentic glomerulonephritis with hematuria and proteinuria
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20
Q

What is Churg-Strauss dz?

A
  • vasculitis caused by WBCs that have been stimulated by ANCA
  • similar to Wegener’s but presents with allergies and asthma and NO renal dz
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21
Q

What is giant-cell (temporal) arteritis?

A
  • m/c type of vasculitis
  • specific to temporal, vertebral, and ophthalmic arteries, accompanied by facial pain and ocular symptoms
  • incidence increases with age
  • associated with HLA-DR4 (genetic component)
  • called polymyalgia rheumatica when ESR is raised
  • presents with granulomatous inflammation in media and intima as well as malaise, fever, weightloss, HA, vision loss, myalgia, and increased ESR with anti-neutrophil Ab’s
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22
Q

What is Buerger dz?

A
  • aka thromboangitis obliterans
  • occlusive inflammatory dz of medium and small aa. in distal extremities
  • m/c before age 35 in smokers
  • presents with intermittent claudication (cramping pains in mm. after exercise then quickly relieved by rest) and ulceration of a digit
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23
Q

What is an aneurysm?

A
  • localized abnormal vessel dilation
  • true: endothelial expansion bonded by all three layers
  • false: no endothelial expansion, instead a leak in a vessel leading to a hematoma covering it
  • dissection: blood enters vessel wall and dissects, forming a hematoma within the wall, then dissecting the layers of the wall, m/c in aorta
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24
Q

What is an abdominal aortic aneurysm (AAA)?

A
  • m/c in males over 50 with atherosclerosis or Marfans’ syndrome
  • usually occur distal to renal aa. and proximal to aortic bifurcation
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25
Q

What is an aortic dissection?

A
  • blood tracks up thru the tunica media, creating a channel

- m/c in hypertensive men 40-60 yrs old

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26
Q

What are the types of hemangiomas?

A
  • hemangioma (angioma, hamartoma): aka birth mark, benign tumor of blood vessels, localized, superficial, m/c on head, neck, liver
  • capillary: m/c on skin, subQ tissue, oral mucosa, “strawberry” type, grows rapidly in first few mths of life then fades by 1-3 yrs
  • cavernous: large and usually cosmetic problem but sometimes in brain
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27
Q

What is a lymph angioma?

A
  • 90% occur in head/neck in kids under 2 yrs
  • m/c in L posterior triangle of neck
  • generally rare, but can be associated with Turner syndrome
  • when large or spaces are present, called cystic hydroma
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28
Q

What is a glomus tumor?

A
  • benign but very painful
  • arise from glomus body cells
  • usually in distal digits, esp. under fingernails
  • excision is curative
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29
Q

What are the characteristics of the miscellaneous benign tumors?

A
  • spider telangectasia: dilation, seen in pregnancy and cirrhosis
  • nevus flammeus: aka port wine stain
  • Osler-Weber-Rendu dz: hereditary hemorrhagic telangectasia
  • bacillary angiomatosis: caused by bacilli of Bartinella species, m/c in HIV pts
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30
Q

What is Kaposi sarcoma?

A
  • low-grade malignancy of endothelial cells

- four forms: chronic (older Ashkenazi male Jews), African, transplant-associated, AIDS-associated

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31
Q

What is an angiosarcoma?

A
  • malignancy of endothelial cells
  • m/c in skin, soft tissue, breast, and liver
  • rapid metastasis
  • positive for CD31 endothelial marker
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32
Q

What is Raynaud’s phenomenon?

A
  • intermittent bilateral attacks of ischemia of the fingers, toes, ears, or nose
  • presents with severe pallor and paresthesia and pain
  • primary: digital pallor => cyanosis => hyperemia, bilateral and symmetrical
  • secondary: associated with atherosclerosis, SLE, and Buerger dz
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33
Q

What are varicose veins?

A
  • affects 20% of population
  • m/c in females in LEs
  • d/t increased venous pressure, age, valve dysfunction
  • pathology: dilated, tortuous, elongated, scarred, calcifications, non-uniform smooth muscle
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34
Q

What is thrombophlebitis?

A
  • 90% occur in deep veins of legs
  • predisposing factors: CHF, neoplastic syndrome, pregnancy, obesity, post-operative, immobilization, and lung adenocarcinoma
  • usually asymptomatic, but may present with edema, cyanosis, heat, pain, and tenderness
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35
Q

What are the heart sounds?

A
  • S1: lub, beginning of systole, closure of bi- and tri-cuspid valves
  • S2: dub, end of systole, closure of aortic and pulmonic valves
  • S3: d/t increased atrial pressure leading to increased flow rates (CHF, dilated cardiomyopathy)
  • S4: presystolic portion of diastole (hypertension, aortic stenosis, ischemic/hypertrophic cardiomyopathy)
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36
Q

What is an opening snap?

A
  • high-frequency early diastolic sound
  • occurs b/w apex and L lower sternal border
  • associated with mitral stenosis
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37
Q

What is valvular heart dz?

A
  • opening problem: stenosis; failure to open completely impedes forward flow
  • closing problem: regurgitation or incompetence; failure to close completely is accompanied by reverse flow
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38
Q

What is valvular stenosis?

A
  • calcification of a valve
  • m/c is aortic
  • causes include rheumatic heart dz (m/c), congenital, senile
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39
Q

What are the causes of regurgitation?

A
  • aortic: rheumatic, infectious, dilation, syphilis, RA, Marfans
  • mitral: prolapse, infectious, injury to papillary mm. or chordae tendinae, calcification of mitral ring (annulus)
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40
Q

What is Takayasu arteritis?

A
  • granulomatous vasculitis of aortic arch
  • m/c in young Asian women under 40 yrs
  • presents with ocular disturbance, weakened pulse, dizziness, and dyspnea
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41
Q

What are the types of congenital aortic stenosis, and the clinical features?

A
  • valvular: most common type, d/t abnormal dvlpmt of endocardial cushions, m/c in males
  • sub-valvular: d/t membrane or fibrous ring around pathway up from LV to aortic valve, m/c in males
  • supra-valvular: associated with idiopathic infantile hypercalcemia
  • clinical features: fainting, dyspnea, angina pectoris, sudden death d/t ventricular arrhythmias
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42
Q

CASE: Pt presents with exertional syncope with convulsion and cyanosis. 1 yr later, develops retrosternal constricting chest pain radiating to L shoulder. History shows rheumatic fever at 14yrs. Dx?

A

Rheumatic heart dz with aortic stenosis

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43
Q

What is mitral valve prolapse?

A
  • aka floppy valve
  • leaflets become enlarged, chordae tendinae become thin and elongated, results in valve prolapse into L atrium
  • linked to Marfans’, Ehlers-Danlos, PKD, and scoliosis
  • clinical features: chest pain, dyspnea, tachycardia, dizziness, mid-systolic click caused by redundant leaflets snapping
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44
Q

What is rheumatic fever?

A
  • multi-system childhood dz following a streptococcal infection
  • d/t inflammatory rxn involving heart, joints, and nervous system
  • m/c in children 9-11 yrs
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45
Q

What is the diagnostic criteria of rheumatic fever?

A
  • major criteria: carditis, polyarthritis, chorea, erythema marginatum
  • minor criteria: previous history of RF, arthralgia, fever
  • Must have 2 major or 1 major + 2 minor for dx
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46
Q

What is the pathology of rheumatic fever?

A
  • myocarditis: fibrinois degeneration of collagen, presents with Aschoff body (granulomatous lesion), Anitschkow cells (chromatin filled nuclei with owl-eye appearance)
  • pericarditis: fibrin deposition results in bread-and-butter appearance, presents with friction rub
  • endocarditis: affects all 4 valves with L ones being more injured
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47
Q

What is Sydenham chorea?

A
  • aka St. Vitus dance
  • rapid, uncoordinated jerking mvmts
  • m/c affects face, feet, and hands
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48
Q

What is mitral stenosis?

A
  • valve orifice is reduced to fixed narrow opening = “fish mouth”
  • if severe, L ventricle is spared and tends to be small and underfilled
  • L atrial pressure is increased => L atrial enlargement => pulmonary hypertension
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49
Q

What is aortic stenosis?

A
  • 2nd m/c valve involved in RHdz
  • diffuse fibrous thickening of the cusps
  • presents with syncope (15%), angina (35%), and CHF (50%)
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50
Q

What is autoimmune endocarditis?

A
  • can occur after strep infection d/t cross-reacting antigens
  • results in verrucae: small vegetations along the valve
  • MacCallum plaques: subendocardial thickening by regugitation, usually in L atrium
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51
Q

What is infective endocarditis?

A
  • microbial invasion of heart valves and endocardium
  • acute: highly virulent bug attack normal valve leading to formation of vegetations and ring abscess, half of pt’s die within weeks
  • subacute: low virulence bug colonizes abnormal valve, slow onset, long course, most recover
  • presents with fever and flu-like symptoms, complications include septicemia, arrhythmias, renal failure, emboli
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52
Q

What are the characteristics of sub-acute bacterial endocarditis?

A
  • causes: alpha-hemolytic strep, staph aureus, e. coli

- clinical signs: splinter hemorrhages, Janeway lesions (palms, soles), Osler’s nodes (raised), Roth’s spots (eye)

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53
Q

What is non-bacterial thrombotic endocarditis (NBTE)?

A
  • vegetation contains fibrin and pits
  • no bacterial involvement
  • comcominant with venous thrombosis, PE, or DIC (hypercoagulability)
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54
Q

What are the causes of myocarditis?

A
  • bacterial: c. diphtheria, chlamydial rickettsia, Lyme dz
  • viruses: coxsackie, CMV, HIV
  • parasites: trypanosoma cruzi (Chaga’s dz)
  • immune: post-viral, rheumatic, SLE, sulfa drugs, hypo- and hyper-thyroidism
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55
Q

What is the pathology of myocarditis?

A
  • interstitial infiltration by mononuclear cells, t-lymphocytes, and macrophages
  • clinical heart failure develops
  • most recover, few die of CHF or arrhythmias
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56
Q

What is cardiomyopathy?

A
  • primary dz of the myocardium
  • classification by cause: inflammatory, immunologic, metabolic, dystrophic, genetic (idiopathic)
  • classification by structural changes: dilated (=> systolic dsfxn), hypertrophic (=> diastoliz dsfxn), restrictive (=> diastolic dsfxn
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57
Q

What are the characteristics of dilated cardiomyopathy?

A
  • mechanism: impaired contractility (systolic dsfxn)
  • cause: alcohol/drugs, pregnancy, nutritional deficiency, anemia, hemochromatosis
  • pathology: collagen deposition results in fibrosis and dilation of all 4 chambers
  • features: ischemic, valvular, hypertensive, or congenital heart dz
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58
Q

What are the characteristics of hypertrophic cardiomyopathy?

A
  • mechanism: impaired compliance (diastolic dsfxn)
  • cause: beta-myosin heavy chain defects, Friedreich ataxia, storage dz’s (genetic) or hypertrophy/fibrosis, infants of diabetic mothers (acquired conditions)
  • features: decreased chamber volume, SV, and diastolic filling, hypertension, aortic stenosis
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59
Q

What are the characteristics of restrictive cardiomyopathy?

A
  • mechanism: impaired compliance (diastolic dsfxn)
  • causes: amyloidosis, sarcoidosis, fibrosis, radiation
  • features: pericardial constriction results in decreased ventricular compliance
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60
Q

What is cardiac tamponade?

A
  • clinical syndrome caused by accumulation of fluid in the pericardial space
  • results in reduced ventricular filling
  • associated with MI, perforation, infective endocarditis, AAA
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61
Q

What are the types of pericarditis?

A
  • serous: RF, SLE, uremia, scleroderma, tumors
  • fibrinous (bread-and-butter) : RF, SLE, uremia, MI, radiation, open-heart surgery
  • purulent: infective, bacterial
  • hemorrhagic: TB, malignancy
  • caseous: TB
62
Q

What is preload?

A
  • the end-diastolic volume (EDV) at the beginning of systole
  • the initial stretching of the cardiac myocytes prior to contraction
  • affected by venous blood pressure and the rate of venous return
63
Q

What is afterload?

A
  • the ventricular pressure at the end of systole (ESP) against which the heart contract to eject blood
  • the greater the aortic/pulmonic pressure, the greater the afterload on the LV/RV
64
Q

What is ejection fraction?

A
  • how much blood the LV pumps out with each contraction
  • normal EF: 55-70
  • < 40 => heart failure or cardiomyopathy
  • > 75 =. hypertrophic cardiomyopathy
65
Q

What are the classifications of hypertension?

A
  • primary (essential): idiopathic, caused by environment of genetic factors, 95% of cases
  • secondary: 5%, caused by renal or endocrine pathologies or exogenous hormones
66
Q

What is hypertension d/t primary hyperaldosteronism?

A
  • excess aldosterone results in renal sodium retention, hypokalemia, and hyperchloremic metabolic alkalosis
  • pts develops increased intravascular volume = hypertension
67
Q

What are the consequences of hypertension?

A
  • heart: hypertrophied myocytes showing nucleomegaly = box car nuclei; onion skinning of arteriole /t necrotizing arteriolitis = organ damage
  • kidneys: renal artery atherosclerosis or stenosis
  • brain: encephalopathy, cerebral edema, microhemorrhages, lacunar infarcts
  • eyes: hypertensive retinopathy
68
Q

CASE: 66 YOF presents with hypertension and sudden, painless, profound loss of vision in the R eye. Dx?

A

hypertensive retinopathy and papilledema

69
Q

CASE: 57 YOM w/ type 2 DM, history of alcohol use, and BP of 168/100 mmHg presents with lab values of blood urea nitrogen at 14 mg/dl, serum creatinine of 1.2 mg/dl, serum glucose of 169 mg/dl, and albumin excretion rate of 250 mg/day. Dx?

A

Diabetic nephropathy (albuminuria, hypertension, and progressive renal insufficiency)

70
Q

What is ischemic heart disease?

A
  • m/c cause of heart dz in the US, leading cause of death
  • causes: atherosclerosis, obstruction, arrhythmia, decreased O2 transport (anemia, lung dz)
  • risk factors: systemic hypertension, smoking, obesity, increasing age, male sex, oral contraceptives, elevated cholesterol, *plasminogen activator inhibitor 1 (PAI-1)
71
Q

What is angina pectoris?

A
  • burning pain in the substernal portion of the chest, radiating to the L arm, jaw, or epigastrium
  • typical (stable): pain on exertion
  • prinzmetal (variant): pain at rest
  • pre-infarction (unstable, accelerated, crescendo): increasing pain with less exertion, may occur during rest or sleep
72
Q

What is myocardial infarction?

A
  • episode of ischemia lasts for a longer period of time, heart muscle cells die
  • leading cause of death in developed nations
  • m/c in males 45+ yrs, and in LV
73
Q

What are the different types of MI by blockage?

A
  • L anterior descending coronary a. (50%): blockage produces infarc of apical, anterior, and antero-septal walls of LV
  • R coronary a. (30%): blockage produces infarct of posterior inferior LV
  • L circumflex coronary a. (20%): blockage produces infarct of lateral LV wall
74
Q

What are the different types of MI by location?

A
  • apical: most damaged from ischemia, m/c site of motion abnormalities
  • global/subendocardial: severe narrowing of all 3 coronary arteries without thrombosis, affects inner third of the LV
  • transmural: involves full LV wall
75
Q

What are the macroscopic stages of MI?

A
  • 24 hrs: recognized by pallor
  • 3-5 days: mottled, sharply outline, central pale-yellow necrotic zone bordered by hyperemic zone
  • 3 wks: myocardium thinned
  • 6-8 wks: good scar
76
Q

What are the microscopic stages of MI?

A
  • 24 hrs: eosinophilic myocytes, coagulative necrosis, edema, loss of sarcolemmal integrity
  • 1-3 days: PMN leukocytes attracted to infarct, muscle cells become necrotic and loose nuclei and striations
  • 5-7 days: phagocytosis of dead muscle, fibroblast and collagen proliferation
  • 3 wks: necrotic debris is removes and replaced by granulation tissue with capillaries, lymphoid cells, macrophages, and fibroblasts
  • 6-8 wks: infarction replaced by solid scar tissue
77
Q

How is MI diagnosed?

A
  • history and exam
  • confirmed by EKG: ST elevation, Q wave formation, T wave inversion, normalization with persistent Q wave
  • increased troponins (sarcolemma), MB-CK (cardiac muscle), and non-specific enzymes liked AST or LDH
78
Q

What is left heart failure?

A
  • failure of LV causes blood back up in the lungs
  • m/c causes include ischemic heart dz, systemic hypertension, mitral/aortic valve dz
  • pt presents with tachycardia, dyspnea, orthopnea, enlarged heart, rales at lung bases; later presents with mitral regurgitation, systolic murmur
79
Q

What is right heart failure?

A
  • failure of RV causes blood back up in body
  • commonest causes include L heart failure, lung dz (cor pulmonale), congenital heart dz
  • pt presents with peripheral edema, hepatomegaly/nutmeg liver, splenomegaly
80
Q

What is cor pulmonale?

A
  • hypertrophy of R ventricle
  • acute causes: massive pulmonary embolism
  • chronic causes: COPD, pulmonary artery dz, chest wall motion impairment
81
Q

What are the classifications of heart failure?

A

1: dyspnea only with vigorous exertion
2: dyspnea with moderate exertion
3: dyspnea with mild exertion, may have mild dyspnea at rest
4: significant dyspnea at rest

82
Q

What are the EKG values?

A
  • P wave: depolarization of R + L atria
  • QRS complex: depolarization of R + L ventricles
  • T wave: ventricular repolarization
  • PR interval: time b/w onset of atrial depolarization to ventricular depolarization
  • QRS duration: length of ventricular depolarization
  • QT internal: length of ventricular depolarization and repolarization
83
Q

How is cortisol controlled in the body?

A
  • hypothalamus releases corticotropin releasing hormone (CRH) => anterior pituitary releases adrenocorticotropic hormone (ACTH) => adrenal cortex releases cortisol
    => cortisol inhibits the anterior pituitary and hypothalamus
84
Q

What is the anatomy of the pituitary gland?

A
  • size: 1 cm, 0.5 gm
  • location: near optic chiasm and CNs 3, 4, 5, 6
  • attached to hypothalamus via stalk
  • anterior: adenohypophysis
  • posterior: neurohypophysis
85
Q

What are the secretions from the anterior pituitary?

A
  • acidophil cells: growth hormone and prolactin (GPA)

- basophil cells: FSH, LH, ACTH, TSH (B-FLAT)

86
Q

What are the secretions from the posterior pituitary?

A
  • oxytocin: causes contraction of uterine smooth muscle

- vasopressin (ADH): concentrates urine

87
Q

What is hypopituitarism?

A
  • occurs when ~75% of parenchyma is lost/absent

- m/c cause is pituitary tumors, also congenital causes

88
Q

What is Reiger’s syndrome?

A
  • autosomal dominant condition resulting in hypopituitarism

- abnormalities of face, teeth, eyes, and pituitary gland

89
Q

What is empty sella turcica syndrome?

A
  • enlarged sella containing a thin, flattened pituitary at the base
  • secondary to defective diaphragm sella
90
Q

What is iatrogenic hypopituitarism?

A

caused by radiation damage to the hypothalamic pituitary axis (HPA) during therapy

91
Q

What is pituitary apoplexy?

A
  • sudden hemorrhage into the pituitary gland, often occurring with pituitary adenoma
  • a neurosurgical emergency characterized by excruciating headace, diplopia, and hypopituitarism
92
Q

What is Sheehan syndrome?

A
  • a hypopituitarism caused by ischemic necrosis
  • m/c d/t severe hypertension caused by postpartum hemorrhage
  • posterior pituitary is less susceptible to ischemic injury, therefore less affected
  • rare with modern OB care
93
Q

What are the symptoms of hypopituitarism?

A
  • dwarfism
  • loss of libido
  • menstrual abnormalities
  • symptoms of hypothyroidism and adrenal insufficiency
94
Q

What is hyperpituitarism?

A
  • excess secretion of pituitary hormones

- m/c cause is pituitary adenomas, also cancer and hypothalamic disorders

95
Q

What is a pituitary adenoma?

A
  • benign neoplasm of the anterior lobe, typically slow-growing
  • can presents with visual field abnormalities d/t close proximity to optic chaism
  • associated with multiple endocrine neoplasia type 1 (MEN-1) and Carney complex, a syndrome of myxomas, pigmentation, and endocrine overactivity
96
Q

How are pituitary adenomas classified?

A
  • cell type: acidophil, basophil, chromophobe
  • size: micro- and macro-
  • function: hormone-producing or hormone-inactive (non-functioning)
97
Q

What are the characteristics of a prolactinoma?

A
  • m/c type of hyperfunctional pituitary adenoma
  • m/c symptomatic in 20-40 YOFs
  • microscopic: weakly acidophilic or chromophobic cells with spheroid nuclei and prominent nucleoli
  • females present with reduced menstruation, fertility, libido, and galactorrhea (milk production w/o pregnancy)
  • males present with ED, reduced fertility and libido, and gynecomastia
98
Q

What are the characteristics of growth hormone adenomas?

A
  • continuously elevated levels of GH stimulate the hepatic secretion of insulin-like growth factor
  • gigantism before closure of epiphyseal plates, acromegaly after closure
  • pt presents with overgrowth of mandible, thickened nose, enlarged hands and feet, gonadal dysfunction, arthritis, and 1/3 have hypertension and cardiomegaly
99
Q

What are the types of GH adenoma?

A
  • densely granulated somatotroph adenoma: contain acidophilic cells arranged in cords and ribbons
  • sparsely granulated somatotroph adenoma: chromophobe cells with spheroid cytoplasmic inclusions called fibrous bodies
100
Q

What are the characteristics of corticotroph adenomas?

A
  • small microadenomas
  • basophilic, densely granulated
  • induces hypercorticism and Cushing’s dz
101
Q

What is the difference b/w Cushing syndrome and dz?

A
  • Cushing dz: hypercortisolism d/t ACTH hypersecretion
  • Cushing syndrome: a condition caused by oversecretion of glucocorticoid hormones from the adrenals resulting in a redistribution of body fat
102
Q

What is Nelson syndrome?

A
  • aka postadrenalectomy syndromy

- the rapid enlargement of a pituitary adenoma that occurs after the removal of both adrenal glands

103
Q

CASE: 37 YOM with history of alcohol abuse presents to ER with seizures. MRI reveals small sellar mass with compression of optic chiasm. Hormonal evaluation was WNL. Histology revealed a chromophobe adenoma with increased mitotic forms. Dx?

A

Non-functioning pituitary tumor

104
Q

What is diabetes insipidus?

A
  • d/t ADH deficiency (from posterior pituitary)

- symptoms: polyuria, polydypsia, high serum sodium (hypernatremia)

105
Q

What are the secretions from the thyroid?

A
  • calcitonin (lowers calcium)
  • thyroxine (T4)
  • triiodothyronine (T3)
  • T4 is converted into T3 in most of the target tissues
106
Q

What is the structure of the thyroid gland?

A
  • follicles lined by cuboidal epithelium and filled with colloid
  • colloid secretes thyroglobulin, from which active T3 and T4 are released
107
Q

What are the congenital anomalies of the thyroid?

A
  • agenesis: absence of thyroid tissue
  • ectopic: thyroid tissue outside the gland d/t abnormal migration during dvlpmt, may be located lateral to jugular veins or in lymph nodes, lingual thyroid = remains at base of tongue if failing to descend during dvlpmt
  • thyroglossal duct cyst: if duct fails to close, a cystic remnant may be seen anywhere along the duct, papillary carcinoma may develop from this cyst
108
Q

What are the different types of thyroid enlargement?

A
  • diffuse: toxic goiter, Graves, Hashimotos, subactue tyroiditis, euthyroid goiter, silent thyroiditis
  • masses: thyroid cyst, benign adenoma, carcinoma
  • multinodular: Plummer’s dz
109
Q

What are the characteristics of euthyroid conditions (non-toxic goiter)?

A
  • normal thyroid function, goiter usually caused by dietary deficiency of iodine
  • m/c in females (8:1), common during adolescence and pregnancy, tends to be familial
  • gland shows hypertrophy and hyperplasia of follicular epithelial cells
110
Q

What are the characteristics of multinodular goiter?

A
  • extreme enlargement, may cause dysphagia or inspiratory stridor, venous congestion of the head/face, and hoarseness
  • non-toxic: most patients are euthyroid (T3, T4, TSH WNL)
  • toxic: many patients eventually develop hyperthyroidism
111
Q

What are the causes of hypothyroidism?

A
  • defective thyroid hormone synthesis
  • inadequate thyroid function: thyroiditis (AI), infiltration (sarcoidosis), surgical resection, or radioiodine
  • inadequate secretion of TSH: pituitary dysfunction (TSH) or hypothalamic dysfunction (TRH)
112
Q

What is endemic goiter?

A
  • congenital hypothyroidism in areas of endemic goiter
  • d/t dietary iodine deficiency in geographical areas like US Great Lakes, Africa, China, Himalayas
  • may be reversed with iodine supplements
113
Q

What is cretinism?

A
  • hypothyroidism seen in infancy or early childhood, caused by deficiency of iodine, m/c in girls
  • symptoms: apathy, weakness, hypothermia, anemia, large abdomens (umbilical hernia), stunted growth, cardiomegaly
  • lab values: low T3 and T4, high TSH
114
Q

What is myxedema?

A
  • hypothyroidism seen in adults with a hypometabolic state caused by low thyroid hormone
  • symptoms: bradycardia, decreased sympathetic activity (cool pale skin), depression, edema of face/hands/feet, constipation, delayed reflexes
115
Q

What is thyroiditis?

A
  • inflammation of the thyroid
  • m/c causes are strep, staph, and pneumococcus, also can be AI
  • pt presents with fever, chills, malaise, painful and swollen neck
116
Q

What is Hashimoto’s thyroiditis?

A
  • m/c cause of hypothyroidism in nonendemic areas of the world
  • m/c in females b/w 25-65 yrs
  • macroscopic: thyroid is enlarged and firm with capsule intact
  • microscopic: follicular destruction, lymphocytic infiltration, presence of Hurthle or Askanazyc cells
  • lab values: low T3 and T4, high TSH
117
Q

What is subactue thyroiditis?

A
  • aka De Quervain’s dz
  • non-suppurative, painful enlargement, m/c in females 30-50 yrs
  • presents with neck pain radiating to jaw, fever, malaise, transient hyperthyroidism (2-6 wks), followed by hypothyroidism (8 wks), and complete recovery
  • macroscopic: thyroid is enlarged and firm
  • microscopic: released colloid d/t follicular destruction leads to granulomatous changes and presence of multinucleated giant cells
118
Q

What is Riedel thyroiditis?

A
  • thyroid is hard and woody
  • m/c in middle aged females
  • presents with gradual onset of painless hard goiter and stridor, dysphagia, and hoarseness
119
Q

What is silent thyroiditis?

A
  • painless inflammation
  • m/c in middle age or post-partum
  • absence of anti-thyroid antibodies, presence of lymphoid infiltrate
  • usually lasts 2-4 months then patients become euthyroid
120
Q

What are the types of hyperthyroidism?

A
  • if symptomatic, called thyrotoxicosis
  • primary: m/c cause of Graves, 95% of cases d/t diffuse hyperplasia
  • secondary: d/t external hormones, pituitary adenoma, ovarian tumor
121
Q

What is Graves disease?

A
  • m/c cause of hyperthyroidism
  • m/c autoimmune condition in the US
  • m/c in females 20-40 yrs
  • symptoms: hyperreflexia, tachycardia, sympathetic overstimulation, increased CO and BP, osteoporosis, exophthalmos
122
Q

What are the changes that take place with Graves disease?

A
  • pathogenesis: IgG antibodies to TSH receptor act as agonists to stimulate TSH and TSI receptors to increased thyroid secretion
  • macroscopic: diffuse, nodular, symmetrical enlargement
  • microscopic: diffuse hyperplasia of epithelial linings of follicles
123
Q

What are the different tumors of the thyroid?

A
  • adenoma: benign, solitary, hyperfunctioning thyroid tumor, m/c occuring in the middle age, histo shows large follicles filled with colloid
  • papillary carcinoma: malignant, firm, white thyroid tumor, m/c thyroid carcinoma, histo shows psammoma bodies with clear nuclei
  • follicular carcinoma: m/c occuring in pt’s 40+ yrs old (rare in children), solitary palpable nodules on physical exam
  • medullary carcinoma: non-capsulated, solid tumor with vascular stroma and eosinophilic amyloid, positive for calcitonin endocrine marker, direct invasion into soft tissues and metastasis into nodes, lung, liver, bones
124
Q

What is the anatomy of the parathyroid gland?

A
  • derives from branchial cleft 3 and 4
  • most people have 4 glands, but numbers vary from 1 to 12
  • composed of chief cells (secrete PTH) and oxyphil cells
125
Q

What is the function of the parathyroid gland?

A

Low levels of ionized (free) calcium stimulate parathyroid gland to release PTH…

  1. Bone: PTH stimulates osteoclasts to resorb bone, increasing serum calcium levels
  2. Kidneys: PTH increases renal tubular reabsorption of calcium, secretion of phosphates, and promotes activation of vitamin D
  3. GI: Activation of vitamin D promotes calcium absorption from food
126
Q

What are the types of hyperparathyroidism?

A
  • primary: persistent production of PTH in the absence of intestinal or renal stimulation, aka autonomous or spontaneous
  • secondary: caused by any condition associated with low serum calcium level, which causes compensatory hyperplasia of the parathyroid
  • tertiary: the development of autonomous parathyroid hyperplasia after longstanding hyperplasia secondary to renal failure
127
Q

What are the characteristics of primary hyperparathyroidism?

A
  • m/c in females 50+ yrs

- pt presents with hypercalcemia, hypophosphatemia, bone dz, and increases serum ionized calcium

128
Q

What are parathyroid adenomas?

A
  • circumscribed, reddish-brown, solitary masses about the size of an olive
  • cystic changes and hemorrhagic areas are common
129
Q

What is primary parathyroid hyperplasia?

A
  • m/c in females, associated with familial hyperparathyroidism or MEN-1
  • all four parathyroid glands are enlarged
  • microscopic: normal glandular adipose tissue is replaced by hyperplastic chief cells arranged in trabecular patterns
130
Q

What is parathyroid carcinoma?

A
  • rare, but occurs in both sexes, m/c b/w 30-60 yrs

- lobulated, firm, non-encapsulated masses often seen with vascular invasion

131
Q

What are the characteristics of secondary hyperparathyroidism?

A
  • m/c in chronic renal failure with decreased phosphate excretion
  • elevated serum phosphate levels directly depress serum calcium levels, thereby stimulation parathyroid gland activity
  • increased chief cells with water clear cells and metastatic calcification of tissues
132
Q

What are the clinical features of hyperparathyroidism?

A
  • hypercalcemia and hypophsphatemia
  • increased PTH => calcium loss from bones
  • increased calcium reabsorption from renal tubules => renal colic and kidney stones, polyuria, polydipsia
  • increased GIT absorption of calcium => peptic ulcers d/t increased gastric secretion d/t hypercalcemia, constipation, pancreatitis
  • increased active vitamin D production
  • bone lesions: osteitis fibrosa cystica => bone pain, bone cysts, pathologic fractures
133
Q

What is hypoparathyroidism?

A
  • decreased secretion of PTH or end-organ insensitivity to it (pseudohypoparathyroidism)
  • characterized by hypocalcemia and hyperphosphatemia
  • clinical features: tingling in hands/feet, muscle cramps, convulsions, depression, cataracts, positive Chvostek sign (tapping along facial nerve) and Trousseau sign (arm cuff with forearm and hand carpal spasm)
134
Q

What is the anatomy of the adrenal glands?

A
  • medulla: chromaffin cells that secrete catecholamines (nor/epinephrine)
  • cortex: zona glomerulosa that secretes aldosterone, zona fasciculata that secretes cortisol, zona reticularis that secretes sex steroid
135
Q

How do the corticoids functions?

A
  • aldosterone (mineralocorticoid): maintains sodium balance by reducing sodium excretion from the body by stimulating sodium reabsorption by the kidney; stimulated by decreased sodium and BP, and increased potassium
  • cortisol (glucocorticoid): maintains blood sugar levels via gluconeogenesis and release into blood, maintains blood volume by preventing water shift into tissues
136
Q

What is congenital adrenal hyperplasia?

A
  • autosomal recessive enzyme deficiency of 21-hydroxylase (P450C21)
  • inability to make cortisol from cholesterol
  • m/c among those of Jewish, Iranian, and Moroccan descent
137
Q

What are the types of congenital adrenal hyperplasia?

A
  • simple virilizing form: female newborns are exposed to excess of androgens in utero, born with fused labia and enlarged clitoris, also short stature, males exhibit no sexual abnormalities
  • salt wasting form: linked to HLA-BW47, impaired aldosterone synthesis, babies develop hyponatreia, hyperkalemia, dehydration, hypotension, and increased renal secretion developing in the first few wks of life, rapidly fatal if untreated with glucocorticoids and mineralocorticoids
138
Q

What are the clinical types of adrenogenital syndrome?

A
  • simple: adrenal hyperplasia with no salt-wasting, females with ambiguous genitalia, males with precocious puberty and enlarged genitalia
  • classic: salt-wasting, adrenal hyperplasia, female phalloid organ, normal male at birth
  • non-classic: m/c, asymptomatic or hirsutism
139
Q

What is Waterhouse-Friederichsen syndrome?

A
  • features: hypotension, shock, DIC, adrenal hemorrhage, d/t severe bacterial infection
  • dx: increased ACTH, decreased cortisol
140
Q

What is Addison’s dz?

A
  • primary chronic adrenal insufficiency
  • d/t failure of adrenal glands to produce androgens and gluco- and mineralocorticoids
  • usually linked to one of four disorders: AI adrenalitis, TB, AIDS, or metastatic cancer
  • m/c in white women
  • presents with lymphoid infiltrations in the adrenal gland and circulating Abs to adrenal antigens
141
Q

What is the pathology of Addison’s dz?

A
  • symptomatic when 90% of the adrenal gland is destroyed
  • macroscopic: glands are pale, irregular, shrunken
  • microscopic: chronic inflammation, fibrosis, lymphoid infiltrates, intact medulla
  • dx: test corticosteroid blood levels after ACTH injection
142
Q

What is secondary adrenocortical insufficiency?

A
  • aka secondary hypoadrenalism
  • caused by cancer, infection, infarction, irradiation of hypothalamus or pituitary
  • no pigmentation b/c melanotropic hormone levels are low, ACTH not increased, no low serum ACTH levels
143
Q

What is an adrenocortical adenoma?

A
  • macroscopic: firm, yellow, encapsulated
  • microscopic: clear, lipid-laden cells in sheets or nests
  • can produce extra cortisol or aldosterone
144
Q

What is an adrenocortical carcinoma?

A
  • rare and aggressive
  • macroscopic: soft, lobulated, necrotic and hemorrhagic changes
  • microscopic: pleomorphic cells or well-differentiated cells, both clear and compact
  • m/c in women
  • metastasize to lung, liver, lymph nodes so poor prognosis
145
Q

What are the three syndromes of hyperadrenalism?

A
  • excess cortisol: Cushing syndrome
  • excess aldosterone: hyperaldosteronism
  • excess androgens: adrenogenital or virilizing syndrome
146
Q

What are the characteristics of Cushing dz?

A
  • primary dz associated with oversecretion of ACTH
  • m/c in women in their 20-30s
  • presents with diffuse adrenal hyperplasia: enlarged cortex, zona fasciculata has large clear lipid-laden cells
147
Q

What are the causes of Cushing syndrome?

A
  • m/c cause in US is chronic corticosteroid administration for immune disorders
  • ACTH secreting pituitary microadenoma: usually causes Cushing’s dz (not syndrome), m/c in 25 yr old females, increased ACTH and cortisol
  • primary adrenal causes: hyperplasia, carcinoma (m/c in children), adenoma (m/c in adult females), decreased ACTH with increased cortisol
  • ACTH secreting conditions: small cell carcinoma, m/c in young boys, presents with increased ACTH and cortisol
148
Q

What is Conn syndrome?

A
  • primary hyperaldosteronism
  • m/c in children and young adults
  • d/t adrenal adenoma or hyperplasia
  • presents with sodium retention and potassium excretion, leading to hypertension and hypokalemia, also alkaline urine is present
  • macroscopic: yellow adenoma
  • microscopic: presence of spironolactone bodies (eosinophilic laminated inclusions)
149
Q

What are the characteristics of a pheochromocytoma?

A
  • chromaffic cell neoplasm that synthesizes and released catecholamines
  • m/c in women, and usually unilateral
  • macroscopic: reddish, encapsulated, spongy, with a central scar
  • microscop: polygonal or spindle-shaped chromaffin cells arranged in nests (Zellballen) and surrounded by “salt and pepper” chromatin
150
Q

What is MEN-1?

A
  • aka Wermer syndrome
  • autosomal domimant
  • 3 Ps commonly involved: parathyroid gland, pancreas, pituitary
151
Q

What is MEN-2?

A
  • aka Sipple syndrome
  • autosomal dominant
  • commonly involves thyroid gland

Tri 4 - Pathology II (21 decks)

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