Patho exam 1 Flashcards

1
Q

Hydrostatic pressure

A

Pressure that drives fluid out of the blood

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2
Q

Osmotic pressure

A

Pressure that drive fluid back into the vessels

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3
Q

Aldosterone

A

Released to lower BP
Regulates BP, bv, increase Na absorption

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4
Q

Hyperaldosteronism

A

Excess aldosterone
Leads to hypernatremia, hypokalemia, hypertension, metabolic acidosis

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5
Q

ADH

A

Anti-pee hormone
Raises BP and BV

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6
Q

RAAS

A

Increase BP by activating agiotensin 2 which activates aldosterone

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7
Q

Hyponatremia

A

Too little Na
Caused by: decreased Na intake, diuretics, vomitting/diarrhea/sweating, too much fluid, CHF or Renail failure

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8
Q

Addison’s

A

Decreased aldosterone, peeing out all the sodium

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9
Q

SIADH

A

Increased ADH, retaining too much water

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10
Q

Hypernatremia

A

Too much Na
Caused by: hypersonic solution, not drinking water, loss of water, diabetes insipidus (excess urination), increased sodium intake

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11
Q

Hyperkalemia

A

Too much K+
Addisions
renal failure
burns/tissue damage (K leaks into blood)
ACE inhibitors

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12
Q

atrophy

A

decrease in size of cell
ex: muscular dystrophy

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13
Q

hypertrophy

A

cardiac muscle that gets bigger and bulkier in disorganized fashion
damages heart

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14
Q

hyperplasia

A

increase the number of cells
beneficial in mammary glands to prep for breast feeding

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15
Q

metaplasia

A

cell type changes during times of stress to resist chemical changes
ex: intestinal metaplasia causes cells in upper repiratory tract to change to be able to resist the acidity of stomach acid

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16
Q

dysplasia

A

disorganized cell growth
cells dont look like each other
not necessarily cancer but can become malignant

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17
Q

ischemia

A

lack of blood flow
cant deliver glucose throughout the body
cant excrete waste

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18
Q

hypoxia

A

lack of oxygen

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19
Q

innate immunity

A

born with
immediate response to harmful agents
nonspecific: macrophages, NK cells, fever, inflammation NOT enought ot contain infection

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20
Q

adaptive immunity

A

develop over time
LYMPHOCYTES
ID, attack, reinforces, and amplifies immunity
delayed response to specific antigens
T and B cells

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21
Q

T cells (cell mediated)

A

protect from infections thatve reached inside cell
actually attacks pathogenic cells

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22
Q

CD4 T cells

A

help macrophages break apart and grab bacteria
help b cells make antibodies (IgG, IgA, IgE)

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23
Q

CD8 T cells

A

cytotoxic
kills infected cell (can kill cancer cells)
phagocytes clean up afterwards

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24
Q

B cells (humoral)

A

-provide immunity in fluid by secreting antibodies to circulate throughout the blood
-antibodies that bind to pathogen block infection
-marks the cell so phagocytes know to destroy it

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25
Q

Mast cells

A

key to inflammatory response: histamine, heparin, serotonin, proteases

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26
Q

effects of histamine

A

increase capillary permeability
vasodilation
bronchoconstriction
increase nasal mucus secretions
stimulates sensory receptors

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27
Q

5 cardinal signs

A

heat
redness
swelling
pain
loss of function

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28
Q

anaphylaxis

A

Type 1 hypersensitivity
EXTREME allergic response
food allergies, antibiotics, latex, insect venom

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29
Q

anaphylaxis symptoms

A

edema, itchiness
hoarseness, wheezing, flushed airway obstruction

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30
Q

Type 1 hypersensitivity

A

IgE
immediate reactions
1st exposure= sensitization
subsequent exposure= serious reaction
contraction of bronchi, vasodilation

31
Q

type 1 hypersensitivity clincal presentation

A

hives, eczema, allergic rhinitis, asthma, anaphylactic shock

32
Q

type 1 hypersensitivity treatment

A

antihistamine
corticosteroids (decrease inflammation)
epinephrine (constricts blood vessels)

33
Q

type 2 hypersensitivity

A

IgM and IgG attach to self-reactive cells
occurs when self-reactive cells arent destroyed while maturing (attack healthy cells)

34
Q

type 2 hypersensitivity: cell lysis

A

membrane attack complex punches holes into cell allowing fluids to flow in and out
cell bursts and dies
incites inflammatory process and destroys basement membrane

35
Q

typer 3 hypersensitivity

A

-mediated by immune complexes
-binding of antigen and antibody forms clumps that don’t get cleared out
-get filtered into the wrong areas
-gets stuck in basement membrane
-Common site: kidney

36
Q

type 3 hypersensitivity clinical presentation

A

chills, fever, rash, urticaria, arthritis
ex: post-strep glomerulonephritis

37
Q

type 4 hypersensitivity

A

mediated by T cells
delayed response: t cells take time to ramp up
antihistamines don’t help because its mediated by T cells
ex: poison ivy

38
Q

passive immunity

A

transferred from another source
ex: mom donates antibodies to babies

39
Q

active immunity

A

own immune system responds to something
ex: antibodies develop in response to infection or vaccine

40
Q

antigen testing

A

tests for antigen from a pathogen
once infection clears, positive result will disappear

41
Q

antibody testing

A

doesn’t indicate infection, indicates exposure (prior illness, vaccine)
maintains positive result even if not sick

42
Q

PCR tetsing

A

detects presence of genetic material of pathogen
amplifies RNA/DNA sample

43
Q

helper T cell deficiency

A

conduct whole immune response
amplifies phagocytosis and tells T & B cells what to do
deficiency= unable to fight pathogen
susceptible to opportunistic pathogens

44
Q

HIV transmission

A

semen, blood, breast milk, contaminated needles, mother to baby

45
Q

untreated HIV

A

low CD4
high Viral load
turns into AIDS in 8-10 years

46
Q

symptomatic HIV

A

flu like symptoms 1-2 weeks post exposure

47
Q

Implications of HIV

A

pregnancy: risk if spreading to child during birth and via breast milk

48
Q

ART therapy

A

reduces viral load to undetectable levels
combo of many HIV meds

49
Q

HIV: Risk of cancer and Opportunisitc infection

A

suppressed immune system causes increased susceptibility to opportunistic infections
unable to fight cancer

50
Q

hypokalemia: cause

A

cushing’s (increase Na+, decreased K)
starvation/vomiting
too much insulin (moves K out)

51
Q

hypokalemia: symptoms

A

Lethargic
Low shallow resp
Lethal cardiac rythms
Lots of Urine
Leg cramps
Limp muscles
Low bp/hr

52
Q

hyperkalemia: symptoms MURDER

A

muscle weakness
urinary output little/none
resp failure
decreased cardiac contraction
early muscle twitch
rhythm changes (peaked T waves, prolonged PR)

53
Q

hypocalcemia: cause

A

decreased PTH (throdiectemy)
decreased intake (lactose intolerance)
decreased vitamin d (helps absorb Ca+)
chronic kidney disease (wastes Ca+)

54
Q

hypocalcemia: symptoms CRAMPS

A

convulsions
reflexes hyperactive
arrhythmias (prolonged QT)
muscle spasms
positive signs
sensation of tingling/numbness

55
Q

hypercalcemia: cause

A

hyperactive PTH
increased vitamin D
cancer that spread to bone (leaks Ca+ to blood)
lithium (impacts PTH)

56
Q

hypercalcemia: symptoms WEAK

A

Weakness of muscle
EKG changes
Absent reflexes/altered mental state/ ab distension
kidney stones

57
Q

metabolic compensation

A

release or pick up H
acidosis: too much H+, so release hypervent
alkalosis: too little H+, pick uphypovent

58
Q

respiratory compensation

A

increase or decrease resp rate
#1 source of acid in body is CO2

59
Q

respiratory acidosis

A

build up of CO2 ( greater than 45)
kidneys compensate by increasing bicarb

60
Q

respiratory acidosis: cause DEPRESS

A

drugs/disease of neuromuscular
edema
pneumonia
respiratory center of brain damaged
emboli blocks gas exchange
spasms of bronchial tubes
sac elasticity of aveolar

61
Q

respiratory alkalosis

A

no enough CO2 (less than 35)
kidneys compensate by decreasing bicarb

62
Q

respiratory alkalosis: cause TACHYPNEA

A

temp increase
aspirin toxicity
controlled mechanical ventilation
hyperventilation
hYsteria
pain/pregnancy (3rd tri)
neurological injuries
embolism and edema
asthma due to hyperventilation

63
Q

metabolic acidosis

A

acid build up in body fluids
increased acid production (diabetic keto acidosis)
decreased acid secretion (renal failure)
resp compensates by hyperventilating to expel CO2

64
Q

metabolic acidosis: ACIDOTIC

A

Aspirin toxicity
carbs not metabolized- lactic acid
insufficient kidneys
diarrhea
ostomy drainage
fisTuals
carbonic anhydrase inhibitors (diuretic)

65
Q

metabolic alkalosis

A

excess loss of acids
resp compensates by hypoventilation to increase CO2

66
Q

metabolic alkalosis cause ALKALI

A

aldosterone production excessive
loop diuretics
alkali ingestion
anticoagulant “citrate”- massive blood transfusion
loss of fluids
Increased sodium bicarb admin

67
Q

characteristics of cancer cells

A

rapid growth
invasive
not encapsulated
high mitotic index
poorly differentiated
metastasis

68
Q

Tumor suppressor

A

behaves as the “breaks”
slows down cell division
repairs DNA mistakes
communicate apoptosis

69
Q

oncogenes

A

mutated proto-oncogenes
promote cancer
accelerated cell division

70
Q

parenoplastic syndrome

A

rare disorders triggered by abnormal immune system response to cancerous tumors

71
Q

paraneoplastic examples

A

Cushings, SIADH, hypercalcemia, hypoglycemia, carcinoid syndrome, polycythemia

72
Q

angiogenesis

A

formation of new blood vessels
tumors give off chemical signals to stimulate angiogenesis to feed the tumor

73
Q

diabetes melitus

A

cause hyponatremia
glucose pulls all the water into the blood which dilutes the sodium content

74
Q

diabetes insipidus

A

excess urination