Pathology Test 3

Front 1

what is the causative factors of REFLUX ESOPHAGITIS

Back 1

the action of the gastric juices is critical to the development of esophageal mucosal injury
1. decreased LES tone
2. CNS depressants
3. hypothyroidism
4. pregnancy
5. alcohol/tobacco
6. presence of sliding hiatal hernia
7. delayed gastric emptying and increased gastric vol.

Front 2

what is Barrett Esophagus a major risk factor for?

what happens

Back 2

1. esophageal adenocarcinoma
2. distal squamous mucosa is replaced by metaplastic epithelium

Front 3

what are the TWO criteria are required for the diagnosis of Barrett Esophagus

Back 3

1. columnar epithelial lining above the gastroesphageal junction
2. intestinal metaplasia of the columnar epithelium

Front 4

what is a morphologically definitive diagnosis for Barrett Esophagus

Back 4

1. presence of intestinal goblet among columnar epithelium
2. DYSPLASIA (pre-malignancy, adenocarcinoma)

Front 5

what are the clinical characteristics of squamous cell carcinoma (esophagus)

Back 5

1. dysphagia
2. obstruction
3. difficulty in swallowing
4. weight loss
5. hemorrhage/sepsis
6. aspiration of food via cancerous fistula

Front 6

in esophageal squamous cell carcinoma:
what are the mutagenic compounds?

Back 6

1. alcohol (polycyclic hydrocarbons, fuel oils, and nitrosamine)
2. tobacco

Front 7

in esophageal squamous cell carcinoma:
where does the esophageal lesions begin

Back 7

1. lesion begin as intraepithelial neoplasm (carcinoma in situ, CIS)
2. PROTRUDING most common morphological pattern

Front 8

what is a characteristic of an adenocarcinoma

Back 8

1. malignant epithelial tumor with GLANDULAR differentiation
2. majority of case arise from BARRETT MUCOSA (distal esophagus)
3. tobacco, obesity, H.pylori are risk factors

Front 9

what is the difference between acute and chronic gastritis

Back 9

inflammation of the gastric mucosa with a prodominant...

1. acute: NEUTROPHILIC infiltrate
2. chronic: LYMPHOCYTE and PLASMA CELL infiltrate

Front 10

what are the etiological factors associated with ACUTE gastritis

Back 10

1. HEAVY NSAID USE
2. INCREASE ALCOHOL USE
3. heavy smoking
4. severe stress
5. uremia
6. cancer chemotherapy

Front 11

what are the etiological factors associated with chronic gastritis

Back 11

1. H. PYLORI (90% of cases)
2. GASTRIC HYPERACIDITY
3. autoimmune
4. alcohol/tobacco
5. radiation

Front 12

why is H.pylori so common in chronic gastritis?
what factors contribute to its efficiency

Back 12

1. gram (-)
2. UREASE produce ammonia to buffer gastric acid
3. produces ADHESIN which allows is to bind to gastric epithelium (more significant in type O blood groups)
4. DOES NOT INVADE GASTRIC EPITHELIUM

Front 13

what are the important morphological changes in chronic gastritis

Back 13

1. REGENERATIVE changes are seen (increased mitosis)
2. INTESTINAL METAPLASIA (columnar absorptive cells)
3. atrophy of glandular epithelium
4. lymphocyte and plasma cells in lamina propia

Front 14

what is peptic ulcer disease and how does it occur

Back 14

1. breach in mucosa of the alimentary tract, extends through muscularis mucosae into the submucosa or deeper
2. occurs in the DUODENUM and STOMACH
3. most duodenal ulcers are near the pyloric ring on the anterior wall
4. gastric ulcers are located mostly along lesser curvature

Front 15

what are the FOUR purposed mechanism for H.pylori role in peptic ulcers

Back 15

1. produces protease, breaks down glycoproteins in gastric mucosa
2. produces phospholipase, damages surface epithelial cells
3. neutrophils releases myeloperoxidase, which produce hypochlorus acid and monochloramine which destroys mammalian cells
4. damaged mucosa release leaks nutrients for H.pylori

Front 16

what are the SIX morphological signs of Crohn's Disease

Back 16

1. STRING SIGN
2. SKIP LESIONS
3. LINEAR ULCER
4. superficial ulceration
5. transmural inflammation
6. noncaseating granulomas

Front 17

what is the difference between Crohn's and Ulcerative Colitis?

Back 17

BOTH:
relapsing inflammatory granulomatous disease

crohn's disease:
1. MAY AFFECT ANY PORTION OF THE GI TRACT
2. mostly involves small intestine and colon

ulcerative colitis:
1. LIMITED TO COLON
2. affecting only mucosa and submucosa (except in severe cases)

Front 18

what are the complications associated with Chronic Crohn's Disease

Back 18

1. fibrosing strictures
2. protein losing enteropathy
3. pernicious anemia and steatorrhea
4. increased incidence of cancer of the GI tract

Front 19

what are the morphological characteristics of Ulcerative colitis

Back 19

1. pseudopolyps
2. serosal surface is NOT involved
3. crypt abscesses formed by collections of neutrophils in crypt lumens
4. mucosal ulceration extending into submucosa
5. epithelial dysplasia may be present

Front 20

what are the clinical features of ulcerative colitis

Back 20

1. BLOODY MUCOID DIARRHEA
2. abdominal cramps relieved by defecation
3. marked by emotional/physical stress
4. toxic megacolon
5. perforation
6. long term complication of UC is GI CANCER!!

Front 21

what is a polyp?
what are the two types of polyps that are associated with the colon and rectum

Back 21

polyp: tumorous mass that protrudes into the lumen of bowel

1. hyperplastic: formed as a result of abnormal mucosal maturation, inflammation or architecture
2. adenomatous polyps: results from proliferation, exhibit dysplasia and are precursors of carcinomas

Front 22

what are the malignant risk associated with adenomatous polyp

Back 22

1. cancer is rare in tubular adenomas smaller than 1cm in diameter
2. cancer risk high in sessile villous adenomas more than 4cm in diamter
3. severe dysplasia, when present, is often found in villous areas

Front 23

what are the factors that cause a high incidence rate in Colorectal Carcinomas

Back 23

1. excess energy intake relative to requirement
2. low content of unabsorbable fibers
3. diet high in refined carbohydrates
4. INTAKE OF RED MEAT
5. lack of protective micronutrients

Front 24

in respect to colorectal carcinoma where does tumors in the PROXIMAL colon portion grow as...?

DISTAL?

Back 24

1. proximal portion tumors tend to grow as POLYPOID EXOPHYTIC masses
2. distal portion tumors tend to grow as ANNULAR, ENCIRCLING lesions (NAPKIN RING constriction around bowel)

Front 25

what is the structural characteristic of the invasive tumors in colorectal carcinoma

Back 25

incite DESMOPLASTIC (fibrous tissue) stromal response making these tumors FIRM and HARD

Front 26

what are the clinical features of colorectal carcinomas (5)

Back 26

1. can be asymptomatic for years
2. DISTAL tumors present with melena, diarrhea, and constipation
3. PROXIMAL tumors present with fatigue, weakness, Fe def anemia
4. tumors of rectum and sigmoid are HIGHLY invasive (BAD!!)
5. Fe deficiency in older males means GI CANCER until proven otherwise

Front 27

when does JAUNDICE occur (5)

Back 27

1. excessive production of bilirubin
2. reduced hepatic uptake
3. impaired conjugation
4. decreased hepatic excretion
5. impaired bile flow

*all unconjugated (insoluble in water, tightly bound to albumin, TOXIC, not excrete in urine)

Front 28

what are some causes of neonatal jaundice

Back 28

1. hereditary hyperbilirubinemias: immature hepatic machinery
2. Crigler-Najjar type 1: gene defect for protein that encodes UDP glucoronsyltransferase (death with 18months)
3. Gilbert syndrome: reduced hepatic bilirubin glucoronidating activity. benign
4. Dubin-Johnson: no cannalicular transfer protein

Front 29

what are the serological diagnosis of HAV

Back 29

1. IgM HAV (antibody in serum appears at ONSET and CONFIRMS diagnosis)
2. IgM decreases after a few months
3. IgG HAV (antibody appears as patient recovers and persist throughout life. conferring resistance)

Front 30

what the characteristic of cirrhosis in the liver?
what is the #1 cause?

Back 30

1. bridging fibrous septa
2. parenchymal nodules
3. total disruption of liver architecture
4. alcoholic liver disease (60-70%) and viral hepatitis (10%)

Front 31

stimuli for synthesis and deposition of collagen in pathogenesis of liver cirrhosis

Back 31

1. inflammatory mediators
2. cytokines
3. disruption of extracellular matrix
4. direct stimulation of stellate cell by toxin (alcohol)

Front 32

what is the major source of excess collagen in cirrhosis

Back 32

perisinusoidal hepatic STELLATE CELLS (Ito cell)

Front 33

what are the three stages of alcoholic liver disease.

Back 33

1. hepatic steatosis
2. alcoholic hepatitis
3. alcoholic cirrhosis

Front 34

what are the clinical features of alcoholic liver disease

Back 34

1. portal hypertension
2. hepatorenal syndrome
3. hepatocellular carcinoma
4. hypoalbuminemia
5. gynocomastia
6. spider angioma

Front 35

what is acute pancreatitis

Back 35

abdominal pain resulting from ENZYMATIC NECROSIS and INFLAMMATION of the pancreas

Front 36

what are the three possible pathways of pancreatic enzyme activation

Back 36

1. pancreatic duct obstruction
2. primary acinar cell injury
3. defective intracellular transport of Proenzymes within Acinar Cell

Front 37

what is the morphology of acute pancreatitis

Back 37

1. interstitial EDEMA
2. fat/parachymal NECROSIS
3. acute inflammatory infiltrate
4. HEMORRHAGE

Front 38

in acute pancreatitis, what will you find in the serum?
what will that lead to...

Back 38

increased serum lipase and amylase:
1. abdominal pain
2. severe pancreatitis
3. DIC
4. fluid sequestration
5. RDS
6. peripheral vascular collapse, SHOCK
7. acute renal tubular necrosis

Front 39

what is chronic pancreatitis

Back 39

1. repeated bouts of pancreatic inflammation
2. continued loss of parenchyma and replacement by fibrous tissue

Front 40

what are the important factors involved in the development of chronic pancreatitis

Back 40

1. protein and cellular debris form DUCTAL PLUGS (calcium carbonate to form stones)
2. alcohol induced oxidative stress leads to protein secretion, cell necrosis and inflammation
3. fibrosis replaces damaged pancreatic tissues

Front 41

what are the clinical features of chronic pancreatitis

Back 41

1. caused by alcohol and overeating
2. mild increase in serum amylase
3. abdominal pain
4. jaundice
5. pseudocyst
6. interstitial fibrosis

Front 42

what are the clinical features of Pancreatic Carcinoma?
what are the two signs?
what is found in the serum?

Back 42

1. Trousseau sign: migratory thrombophlebitis, excess platelet aggregating factors and procoagulants from the tumor
2. Carvoisier Sign: palpable distend gallbladder
3. elevated CA 19-9 and CEA in serum

60% occur in head of pancreas and causes an obstructive jaundice

Front 43

what are the MORPHOLOGICAL characteristics of Pancreatic Carcinoma

Back 43

1. practically all are adenocarcinoma, moderate to poor, aggressive and infiltrative
2. may secrete mucin
3. desmoplastic reaction
4. grey-white gritty tissue mass

Front 44

in pancreatic carcinoma what is suppressed at intermediate stages?
late stages?

Back 44

inactivation of...
1. intermediate: p16 tumor suppressor gene
2. late: p53, SMAD4 (DPC4), BRCA2 tumor suppressor gene

Front 45

what is an atheroma?
where do they occcur?

Back 45

1. elevated focal intimal fibrofatty plaque
2. yellow-white in appearance
3. protruding into lumen

occur at point of arterial branching and around Ostia of branches of aorta

Front 46

what are some complications of atheroma

Back 46

1. calcification
2. ulceration
3. thrombosis
4. intraplaque hemorrhage

may cause embolization, total occlusion, or aneurysm

Front 47

what is a theory of development of atheroma

Back 47

reaction to injury due to hypertension, DM, hyperlipidemia, smoking, etc.

1. increase permeability to plasma lipids, foam cell infiltration of subintimal space and collagen deposition

Front 48

what are THREE clinical features of atherosclerosis

Back 48

1. narrowing of lumen (ischemia)
2. predisposed to thrombosis (occlusive or emboli)
3. weakening of wall (aneurysm of abdominal aorta)

Front 49

what are the three diseases that is defined by thickening and loss of elasticity of arterial walls

Back 49

1. atherosclerosis
2. arteriolosclerosis
3. Monckeberg's arteriosclerosis

Front 50

what are some clinical pathologies that can be seen with ischemic heart disease

Back 50

1. angina pectoris
2. MI
3. silent ischemia (no angina, no pain)
4. chronic ischemic heart disease
5. sudden cardiac death (SCD)

Front 51

what is angina pectoris?
what are the THREE types of angina?

Back 51

angina pectoris: chest pain due to myocardial ischemia, WITHOUT FRANK INFARCTION

1. stable: short duration (15min), exertion induced and relieved with rest
2. unstable: more severe pain and longer, attacks occur at rest
3. prinzmetal angina: pain occurs at rest, may be caused by ECG change and coronary artery spasm

Front 52

what does ischemia indicate in MI

Back 52

1. coagulative necrosis of myocardial fibers
2. leads to loss of normal conduction and contraction
3. MI usually involve LV
4. RV is involved if LV infarct is SEVERE

Front 53

what are the lab diagnosis for MI

Back 53

1. CARDIAC TROPONIN I: as sensitive and more specific than CK-MB. (rises within 4-8hrs of attack, remains elevated for 7-8days)
2. CK-MB: marker for MI, (rises 4-8 hrs of attack, normal within 48hrs)
3. elevated LDH and SGOT

Front 54

what are the TWO criteria for classifying MI

Back 54

1. Depth: TRANSMURAL (full thickness of wall, associated with thrombosis) and SUBEPITHELIAL (inner 1/3 or 1/2 of wall, NO thrombosis)

2. location/coronary artery involvement

Front 55

what is the usual cause of sudden cardiac death?

what is the most common cause of death among hospital patients with acute MI?

Back 55

1. ventricular arrhythmias

2. cardiogenic shock

Front 56

what does CHF cause

Back 56

1. >40% of LV infarcted
2. decreased contractility
3. abnormal LV wall motion
4. REDUCE CARDIAC OUTPUT

Front 57

what are the TWO causes of cardiac failure

Back 57

1. inefficiency of myocardial contraction (pump failure)
2. abnormal load (increased work)

Front 58

what are FOUR complications leading to intrinsic pump failure

Back 58

1. myocardial ischemia (CAD)
2. cardiomyopathy
3. myocarditis
4. impaired compliance myocardium
5. rhythm disorders (severe)

Front 59

what are THREE complications leading to increased load

Back 59

1. increased pressure load
2. increased volume load
3. increase debit of general circulation

Front 60

what are FOUR the compensatory mechanism in heart failure

Back 60

1. hypertrophy of myocardium
2. increased blood volume (RAA)
3. increased sympathetic tone
4. compensatory increase in RBC

Front 61

what causes clinical manifestations of heart failure

Back 61

1. increased intravascular VOLUME and PRESSURE
2. extravasation of fluid in LUNGS, other organs and periphery

Front 62

what are the FOUR different types of aneurysms

Back 62

1. fusiform
2. saccular
3. dissecting
4. berry

Front 63

what type of aneurysm is common with atherosclerotic aneurysms

Back 63

1. fusiform and saccular
2. usually in abdominal aorta
3. may produce thrombi and emboli
4. renal artery flow and blood flow to lower limbs may be occluded

Front 64

what happens during syphilitic aneurysm?
type of aneurysm?

Back 64

1. saccular or fusiform
2. ischemic injury of elastic fibers and smooth muscle of media of aorta
3. dilatation of AV ring leading to LV overload and hypertrophy (cor bovinum)
4. obliterative endarteritis of vasa vasurum (perivascular cuff of plasma cell infiltrates)

Front 65

what happens during dissecting aneurysm?
what is a more common cause in patients?

Back 65

1. medial necrosis in muscular layer of aorta
2. marfan syndrome and lathyrism

idiopathic cystic medial necrosis

Front 66

what are the TWO types of dissecting aneurysms?

what are the effects of dissecting aneurysm

Back 66

type A: ascending aorta
type B: descending aorta ONLY

1. rupture (hemorrhage)
2. extension of dissection (renal and mesenteric infarct)
3. disruption of aortic valve (regurgitation)

Front 67

what is giant cell arteritis

Back 67

1. granulomatous inflammation of med/sm arteries (cranial and temporal arteries usually affected)
2. thick/fibroses vessel walls and narrowing of lumen
3. causes headache, fever, anemia, musculoskeletal symptoms

SUDDEN BLINDNESS!!

Front 68

what is Takayasu disease (pulseless disease)

Back 68

1. granulomatous inflammation of med/lg arteries. strong predilection for aortic arch and branches (narrow and destruction)
2. common in women
3. ischemic symptoms in arms and neck
4. DIMINISHED upper extremity PULSES

Front 69

what is polyarteritis nodosa

Back 69

1. necrosis of small and medium arteries throughout body (ischemia of multiple organs and tissue)
2. FIBRINOID NECROSIS
3. NEUTROPHIL INFILTRATE
4. fibrotic thickening and aneurysm formation

Front 70

what is anti neutrophil cytoplasmic antibodies?
how is it used to diagnose?

Back 70

1. auto-antibodies directed against enzymes mainly found within granules in neutrophils
2. cytoplasmic-ANCAs: target antigen is proteinase 3 (wegeners)
3. perinuclear-ANCAs: target is myeloperoxidase (PAN and Churgs-Strauss)

Front 71

what is Churg Strauss Syndrome

Back 71

1. allergic and granulomatous vasculitis
2. mainly lesions of the lungs
3. eosinophilia and association with asthma and allergic rhinitis

Front 72

what is wegeners granulomatosis

Back 72

1. vasculitis with necrotizing granulomas in URT, lungs and kidneys
2. saddle nose deformation
3. lungs: cough, dyspnea, HEMOPTYSIS
4. kidneys: necrotizing glomerulitis and crescentic glomerulonephritis

Front 73

what is thromboangiitis obliterans (buergers)

Back 73

1. segmental inflammation of med/sm arteries and veins (extremities w/ adj nerves...no pain)
2. intermittent claudication
3. ischemia cause tissue ulcer and gangrene

Front 74

what is mucocutaneous lymph node syndrome (kawasaki)

Back 74

1. acute febrile illness in children
2. 20% associated with coronary arteritis and aneurysm formation
3. causes producing thrombosis, rupture and CHILDHOOD MI

Front 75

what is phlebo-sclerosis

Back 75

1. chronic varicosity causes fibrosis and calcification of veins

Front 76

what is the difference between phlebothromobosis and thrombophlebitis?
etiology?

Back 76

1. phlebothromobosis: thrombus in veins
2. thrombophlebitis: inflammation of veins

etiology:
1. venous stasis
2. hypercoagulable states

Front 77

what is telangiectasias

Back 77

1. developmental anomaly
2. present as central dilated vessel with radiating fine capillaries
3. not true tumor appearing as abnormal dilatation of preexisting small vessels

Front 78

what are the FOUR type of vascular growths

Back 78

1. nevus flammeus
2. port wine stain: sometimes associated with encephalo-trigeminal angiomatosis
3. hereditary hemorrhagic telangiectasia: skin, mucous membrane mouth, GI, respiratory and urinary tract
4. spider telangiectasia: liver disease association

Front 79

what is a hemangioma?
what are the two types

Back 79

benign tumor of capillaries

1. capillary hemangioma
2. cavernous hemangioma (cystic hygroma)

Front 80

what is a Kaposi sarcoma

Back 80

low grade malignant tumor

1. pleomorphic spindle shaped cells
2. slit like vascular spaces filled RBC

*classic, transplant KS, AIDS KS

Front 81

what is the most damaging aspect of rheumatic heart disease

Back 81

endocarditis: platelets and fibrin in the endocardium (vegetation)

fibrinoid necrosis

Front 82

what is the pathognomonic (specific) feature of acute rheumatic carditis

Back 82

myocarditis: myocyte necrosis with development of ASCHOFF BODIES

(found in interstitial fibrous tissue of heart, joints, tendons, and other)

Front 83

what is present in the early and late stages of rheumatic heart disease

Back 83

1. early: aschoff nodule consists only of fibrinoid necrosis and inflammatory cells
2. late: becomes nonspecific hylinized scar

Front 84

what are the etiology of hypertension

Back 84

essential HTN: 90% cases no cause found

secondary HTN: 10% well known causes
1. cardiovascular
2. renal
3. endocrine
4. pregnancy
5. sleep apnea
6. drug induced

Front 85

morphologically what is seen in myocarditis

Back 85

1. macro: pale and flabby myocardium with FOUR chamber dilatation and diffuse hemorrhagic mottling (mural thrombi)
2. micro: interstitial edema/fibrosis, mononuclear cell infiltrates (degeneration and necrosis)

chronic: DILATED CARDIOMYOPATHY

Front 86

what is the definition of cardiomyopathy

Back 86

disorder of the heart MUSCLE in the ABSENCE of ischemic, hypertensive, valvular, pericardial or congenital mechanisms of the myocardial disease

Front 87

what is the most common type of cardiomyopathy

Back 87

dilated cardiomyopathy (DCM): congestive cardiomyopathy

1. FOUR chamber dilatation
2. systolic and diastolic dysfunction
3. scattered myocyte atrophy, interstitial fibrosis, mononuclear infiltrate

Front 88

what is the definition of aortic stenosis?

morphology

Back 88

obstruction of LV outflow during SYSTOLE caused by valvular obstruction

HYPERTROPHY
fibrosis and calcification after RHD (thickened)

Front 89

what are the hemodynamic affects of aortic stenosis

Back 89

1. low arterial BP
2. concentric hypertrophy of LV
3. MI and CHF
4. thromboembolism
5. arrhythmia and sudden death

Front 90

what are the signs and diagnosis of aortic stenosis

Back 90

1. angina pectoris
2. dyspnea
3. syncope

systolic murmur and thrill

Front 91

what is the definition of aortic regurgitation

Back 91

abnormal leak or retrograde flow of blood from aorta back into LV during DIASTOLE

Front 92

what are the hemodynamic effects of aortic regurgitation

Back 92

1. LV volume overload
2. DIALATATION of ascending aorta
3, regurgitated stream of blood cause JET LESIONS
4. eventually will lead to MR and PHT