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Patho exam 1 Flashcards

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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
Mast cells
key to inflammatory response: histamine, heparin, serotonin, proteases
26
effects of histamine
increase capillary permeability vasodilation bronchoconstriction increase nasal mucus secretions stimulates sensory receptors
27
5 cardinal signs
heat redness swelling pain loss of function
28
anaphylaxis
Type 1 hypersensitivity EXTREME allergic response food allergies, antibiotics, latex, insect venom
29
anaphylaxis symptoms
edema, itchiness hoarseness, wheezing, flushed airway obstruction
30
Type 1 hypersensitivity
IgE immediate reactions 1st exposure= sensitization subsequent exposure= serious reaction contraction of bronchi, vasodilation
31
type 1 hypersensitivity clincal presentation
hives, eczema, allergic rhinitis, asthma, anaphylactic shock
32
type 1 hypersensitivity treatment
antihistamine corticosteroids (decrease inflammation) epinephrine (constricts blood vessels)
33
type 2 hypersensitivity
IgM and IgG attach to self-reactive cells occurs when self-reactive cells arent destroyed while maturing (attack healthy cells)
34
type 2 hypersensitivity: cell lysis
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
typer 3 hypersensitivity
-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
type 3 hypersensitivity clinical presentation
chills, fever, rash, urticaria, arthritis ex: post-strep glomerulonephritis
37
type 4 hypersensitivity
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
passive immunity
transferred from another source ex: mom donates antibodies to babies
39
active immunity
own immune system responds to something ex: antibodies develop in response to infection or vaccine
40
antigen testing
tests for antigen from a pathogen once infection clears, positive result will disappear
41
antibody testing
doesn't indicate infection, indicates exposure (prior illness, vaccine) maintains positive result even if not sick
42
PCR tetsing
detects presence of genetic material of pathogen amplifies RNA/DNA sample
43
helper T cell deficiency
conduct whole immune response amplifies phagocytosis and tells T & B cells what to do deficiency= unable to fight pathogen susceptible to opportunistic pathogens
44
HIV transmission
semen, blood, breast milk, contaminated needles, mother to baby
45
untreated HIV
low CD4 high Viral load turns into AIDS in 8-10 years
46
symptomatic HIV
flu like symptoms 1-2 weeks post exposure
47
Implications of HIV
pregnancy: risk if spreading to child during birth and via breast milk
48
ART therapy
reduces viral load to undetectable levels combo of many HIV meds
49
HIV: Risk of cancer and Opportunisitc infection
suppressed immune system causes increased susceptibility to opportunistic infections unable to fight cancer
50
hypokalemia: cause
cushing's (increase Na+, decreased K) starvation/vomiting too much insulin (moves K out)
51
hypokalemia: symptoms
Lethargic Low shallow resp Lethal cardiac rythms Lots of Urine Leg cramps Limp muscles Low bp/hr
52
hyperkalemia: symptoms MURDER
muscle weakness urinary output little/none resp failure decreased cardiac contraction early muscle twitch rhythm changes (peaked T waves, prolonged PR)
53
hypocalcemia: cause
decreased PTH (throdiectemy) decreased intake (lactose intolerance) decreased vitamin d (helps absorb Ca+) chronic kidney disease (wastes Ca+)
54
hypocalcemia: symptoms CRAMPS
convulsions reflexes hyperactive arrhythmias (prolonged QT) muscle spasms positive signs sensation of tingling/numbness
55
hypercalcemia: cause
hyperactive PTH increased vitamin D cancer that spread to bone (leaks Ca+ to blood) lithium (impacts PTH)
56
hypercalcemia: symptoms WEAK
Weakness of muscle EKG changes Absent reflexes/altered mental state/ ab distension kidney stones
57
metabolic compensation
release or pick up H acidosis: too much H+, so release hypervent alkalosis: too little H+, pick uphypovent
58
respiratory compensation
increase or decrease resp rate #1 source of acid in body is CO2
59
respiratory acidosis
build up of CO2 ( greater than 45) kidneys compensate by increasing bicarb
60
respiratory acidosis: cause DEPRESS
drugs/disease of neuromuscular edema pneumonia respiratory center of brain damaged emboli blocks gas exchange spasms of bronchial tubes sac elasticity of aveolar
61
respiratory alkalosis
no enough CO2 (less than 35) kidneys compensate by decreasing bicarb
62
respiratory alkalosis: cause TACHYPNEA
temp increase aspirin toxicity controlled mechanical ventilation hyperventilation hYsteria pain/pregnancy (3rd tri) neurological injuries embolism and edema asthma due to hyperventilation
63
metabolic acidosis
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
metabolic acidosis: ACIDOTIC
Aspirin toxicity carbs not metabolized- lactic acid insufficient kidneys diarrhea ostomy drainage fisTuals carbonic anhydrase inhibitors (diuretic)
65
metabolic alkalosis
excess loss of acids resp compensates by hypoventilation to increase CO2
66
metabolic alkalosis cause ALKALI
aldosterone production excessive loop diuretics alkali ingestion anticoagulant "citrate"- massive blood transfusion loss of fluids Increased sodium bicarb admin
67
characteristics of cancer cells
rapid growth invasive not encapsulated high mitotic index poorly differentiated metastasis
68
Tumor suppressor
behaves as the "breaks" slows down cell division repairs DNA mistakes communicate apoptosis
69
oncogenes
mutated proto-oncogenes promote cancer accelerated cell division
70
parenoplastic syndrome
rare disorders triggered by abnormal immune system response to cancerous tumors
71
paraneoplastic examples
Cushings, SIADH, hypercalcemia, hypoglycemia, carcinoid syndrome, polycythemia
72
angiogenesis
formation of new blood vessels tumors give off chemical signals to stimulate angiogenesis to feed the tumor
73
diabetes melitus
cause hyponatremia glucose pulls all the water into the blood which dilutes the sodium content
74
diabetes insipidus
excess urination

Patho (5 decks)

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