Alexis HD Flashcards

1
Q

Acute Inflammation Stages

A

-Vasodilation
-Increased vascular permeability
-Edema
-Leukocyte (neut) recruitment
-Rolling, pavementing, migrating
-Leukocyte activation
-Phagocytes, killing, degradation

VASO = EDEMA = LEUKOCYTES

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2
Q
A

GRANULATION TISSUE

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2
Q

What makes FGF?

A

MACS
-make cytokines, chemokines, interleukins

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3
Q

Cancer In Men (Incident/Death)

A

Incidence: Prostate

Death: Lung

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4
Q

Main Cause of this Cancer?

A

Lung Cancer = Smoking

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5
Q

Cancer In Women (Incident/Death)

A

Incidence: Breast
Death: Lung

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6
Q
A

Intestinal metaplasia and esophagus
cancer at gastroesophageal junction
-Circle in middle is the cancer, middle is metaplasia
-Gastric gases squirted up due to GERD

NORMAL - METAPLASIA - CANCER

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7
Q
A

Atherosclerosis and Thrombosis

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8
Q

Hereditary Hemochromatosis

A

-Mutant HFE gene product involved in regulating iron uptake via hepcidin
-Decreased hepcidin causes increased iron uptake causes hemochromatosis with cirrhosis

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9
Q

EDEMA

A

Increased fluid in interstitial spaces (bc of increased hydrostatic pressure or decreased plasma osmotic pressure)

Cancer in lymph nodes –> edema

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10
Q

What is involved in anticoagulation?

A

Heparin like molecules

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11
Q

What is involved in anti platelet?

A

Prostacyclin and Nitric oxide

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12
Q

Prothrombotic Properties of Injured or Stimulated Endothelium

A

Platelet adhesion to subendothelial collagen via von Willebrand factor
-activates extrinsic clotting pathway via tissue factor

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13
Q

Pulmonary Thromboembolism

A

Deep leg vein thrombi to RIGHT side of the heart

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14
Q
A

Pulmonary thromboembolus (circled) obstructing pulmonary artery and consequent hemorrhagic infarct of lung
distally

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15
Q

What is an infarct?

A

-Ischemia causing tissue death
-Coagulative necrosis

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16
Q

Septic Shock

A

-Triggered by multiple microbial constituents
-Activate Macs, neutros, endothelium
-Vasodilation, endothelial damage (DAD DIC)

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17
Q

Which layer in the tunica does atherosclerosis affect?

A

INTIMAL thickening (intima)

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18
Q

What does atherosclerosis mean?

A

Lipid rich HARDENING / GRUDGE

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19
Q

Plaque Complications

A

-Stenosis
-Rupture: embolism
-Hemmorrhage: occlusion
-Thrombosis: occlusion and embolism
-Aneursym

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20
Q
A
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21
Q
A

Thromboembolism occluding arterial lumen

22
Q

Coagulative

A

Ischemia / Infarcts

23
Q

Liquifactive

A

Focal bacteria infections, abscesses

24
Q

Fibrinoid

A

AgABC complexes, radiation

25
Q

Caseous

A

Tuberculosis

26
Q

Events in Cell Injury/Death

A
  1. Mitochondria
    -Hypoxia, toxins, radiation
    -Failure of ox. phos.
    -Decrease ATP generation
  2. Plasma
    -Failure of ATP dependent NA Pumps
    -Na rushes in, water follows, cell swells
  3. Lysosomal
    -Enzymatic digestion of cell components
27
Q

Examples of Apoptosis?

A

Sloughing of dead endometrial cells

-Embryogenesis
-Involution: menstruate, post lactation
-Neuts and lymphs in resolving inf
-Killer T cell activation (viral)
-DNA damaged cells

28
Q

Hypertrophy

A

INCREASE IN CELL SIZE

29
Q

Hyperplasia

A

INCREASE IN NUMBERS OF CELLS

30
Q

Examples of hyperplasia?

A

lactating breast in a woman’s last trimester of pregnancy

31
Q
A

metaplasia transitions into neoplasia in the esophagus

32
Q

Macrophages create ___ in inflammation

A

fibroblasts

33
Q

Edema: difference between exudate and transudate

A

-Exudate has PROTEIN AND fluid leakage
-Transudate has just fluid leakage

34
Q

what is the best target for carcinogens grow

A

I am assuming to stop cancer growth.
I didn’t know the answer BUT two of the options were to target bone marrow cells or toipent cells.

35
Q
A

Macrophages

36
Q

Another question asked along the lines of chronic inflammation and viral infection. The main point is that chronic inflammation and viral infection both consists of ____

A

LYMPHOCYTES

37
Q

Acute vs Chronic Inflammation

A

Chronic has scarring fibrosis

38
Q

Q will be: what is NOT apart of the outcome in chronic inflammation?

A

Usual Suspects
-TB
-Sarcoidosis
-Fungi
-Foreign bodies
-Protozoans/parasites

39
Q
A

Liemyosarcoma invading wall of myometrium

-Circle part is the invasion, malignant tumor of smooth muscle cells

40
Q

Benign vs Malignant

A

-Benign: not harmful, not cancer, don’t invade, don’t spread, slow growth

-Malignant: cancer, invade, spread, quick growth

41
Q

Tumor

A

Lump or mass

42
Q

Neoplasia

A

new shape or new mold, just NEW thing that wasn’t there before, new growth (could be benign or malignant)

43
Q

Carcinoma

A

all cancer, derived from epithelial cells

44
Q

Sarcoma

A

all cancer, derived from connective tissue or messenchymal tissue

45
Q

Difference between oncogenes and tumor suppressor

A

Oncogenes: ONE mutation in alleles to be mutated (TOO MUCH GAS), GOF!

Tumor suppressor: TWO mutations to cause mutation (NO BRAKES), LOF!

46
Q

What is a preneoplastic predisposition?

A

Cirrhosis!

-unhealing wounds, endometrial hyperplasia, metaplasia, adenoma, ulcerative colitis

47
Q

What stage and grade has the worst prognosis?

A

-Grade: how ugly is it, how much it resembles tissue it is supposed to be (less recognizable = HIGHER grade)
-Stage: how far has it gotten

HIGH STAGE = WORSE

48
Q

What does “atherosclerosis” mean?

A

“Athero” porridge or gruel
“sclerosis “ hardening

49
Q

Sporadic colon cancer

A

Familial adenomatous polyposis (same pathway)

50
Q

Autosomal Recessive disorders

A

-Only manifest when both alleles of a gene are mutant
-Complete penetrance and uniform expression
-Often involve enzymes

EX: Hereditary Hemochromatosis

51
Q

Autosomal Dominant Disorders

A

-Manifest in heterozygous state
-Reduced penetrance and variable expressivity
-Usually effects non-enzyme proteins, receptors and structural proteins

EX: Familial hypercholesterolemia

52
Q

Edema: colloid vs hydrostatic pressure

A