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398 pharm/patho > midterm > Flashcards

midterm Flashcards

1
Q

Hydropic

A

(reversible cell injury)

  • accum of water
  • *1st manifestation of most forms of rev cell injury
  • results from malfunction of Na-K pumps (Na ions flow into cells…H2O follows–>
  • generalized swelling in cells of whichever organ is effected; megaly: increase in size/weight; ie: splenomegaly during mono
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2
Q

Intracellular accumulations

A

(reversible cell injury)
could happen from genetic disorder or enzymes missing..
1 excessive amts of normal intracell substances (ie proteins, lipids, carbs etc)
2 accum of abnormal sub pro by cell bc of issues (cellular stress–>accumulation of (abnormal) broken down proteins)
3 accumulation of pigments and particles that cell is unable to degrade (ie newborns w imm liver & increased RBC (which the liver can’t process)–> accumulation of bilirubin–> discoloration of skin

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3
Q

Cellular adaptions: responses to increase/decrease in functional demand…

A

atrophy: cells shrink and reduce their differentiated function; protective mechanism for E conservation, but negative if goes on too long; ie: during ischemia, starvation, differences w/ endocrine processes
hypertrophy: increase in cell size accompanied by augmented functional capacity (bc working harder); ie cells that can’t reproduce and undergo mitotic div would hypertrophy
hyperplasia: increase in # of cells by mitotic division
* can have hypertrophy/plasia at same time, ie pregnancy- breast tissue undergoes both; ie: hypertension

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4
Q

cellular adaptions: responses to persistent injury

A

metaplasia: replacement of one differentiated cell type w/ another; ie: smokers w/ chronic irritation of bronchia mucosa–> change of cells to handle the stress
dysplasia: disorganized appearance of cells bc of abnormal variations in size, shape and arrangement
* HPV can have either - hopefully doc intervenes at metaplasia, before dysplasia can begin
* either can lead to cancerous cells

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5
Q

Irreversible cell injury

A

Necrosis & apoptosis

  • both are processes that lead to cell death
  • could have both together in same process (heart attack)
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6
Q

necrosis

A
  • consequence of external injury or ischemia (inadequate blood supply to an organ or part of the body, especially the heart muscles)
  • characterized by cell rupture caused by disruption of plasma/cell membrane–> intracell contents spill out–> inflammation;
  • take lab values of spillage to monitor the prob
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7
Q

apoptosis

A
  • can happen as natural progression of cell life or if signals sent
  • no breaking of membrane/spillage/inflammation
  • “organized cell death”
  • norm process
    ie dementia pt - change in CT scan shows atrophy of brain related to apoptosis
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8
Q

nutritional cell injuries

A

deficiencies (ie iron, vit D)
&
excess (ie Na excess = hypertension; fat excess = obesity…diabetes)

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9
Q

chemical cell injuries

A 
free radicals
heavy metals (ie lead)
toxic gases (ie CO2 poisoning)
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10
Q

Physical & Mechanical cellular injuries

A
  • temp extremes: too hot, heat stroke; too cold, frost bite
  • abrupt changes in atmospheric pressure: altitude increase can lead to cell injury if they don’t adapt; altitude decrease and lead to N imbalance “the bends
  • abrasion…trauma
  • electrical: ie burns
  • radiation: can cause damage…1 directly to DNA; 2 creates free radicals –> cell dysfunction–>necrosis
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11
Q

Infectious & Immunologic cellular injuries

A

~Bacteria:
- endotoxins: toxins inside bacteria released when bacteria killed (plasma wall broken)–> wreaks havoc on body
- exotoxins: released/excreted by bacteria as a protective mechanism to stay alive (ie cholera/dyptheria)
~Virus: invades cell and replicates
~Indirect immunologic responses too

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12
Q

Rel bw host and pathogen:

symbiosis, mutualism, and commensialism

A

benefit human/no harm to microorganisms
benefit to both
benefit microorganisms/no harm to human

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13
Q

pathogenicity

A

benefits organism/harms human; ability of microorganisms to cause disease

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14
Q

toxigenicity

A

ability of microbe to produce endo/exo toxins; thought to be more virulent

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15
Q

immunogenicity

A

ability of pathogen to induce immune response (toxins, enzymes, mobility etc)

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16
Q

virulence

A

how severe of a disease a mircroorg may cause

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17
Q

endo v exo toxins

A

endo: toxins inside that are released when cell wall ruptured (organism is killed)
exo: toxins excreted by org (ie: tetanus)

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18
Q

bacteria

A

single cell; rigid wall; no internal organelles
cocci/bacilli/spiral
gram +, -, acid fast (resist stain)
aerobic or anaerobic

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19
Q

fungi

A

eukaryotic; w/ organelles- complex structure; rigid wall; often part of normal flora, but cause prob when body’s defense compromised (ie: mycotic infection); located superficial/cutaneous, subcutaneous (ulcer/abcess), and systemic

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20
Q

parasites

A

best themselves w/ host and live off of/benefit from them; protozoa (single cell); helminths (round/flat worms); arthropods (lice/ticks); **most often on skin/in GI tract

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21
Q

viruses

A

most common affliction;
simple microorg-no metabolism and can’t reproduce independently; must infect host to replicate
hard to treat/prevent bc of ability to adapt
can bypass defense mech bc they dev intracellularly (which gives them protection)

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22
Q

incubation stage

A

period from initial exposure to onset of 1st symptoms; contagious before you knew you had it

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23
Q

prodromal

A

occurrent of initial symptoms (mild)

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24
Q

illness

A

pathogen multiplies rapidly; immune/inflamm responses triggered; dev symptoms specific to pathogen

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25
Q

convalescence

A

1- immune/inflamm systems have successfully removed agent and symptoms go down
2- latent phase w/ resolution until reactivation
3- fatal

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26
Q

subclinical

A

pt functions normally even tho disease processes are well established (subclinical hypertension)

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27
Q

clinical manifestation of infection

use for assessment of patient

A

*majority of s/s from inflammation
nonspecific s/s: fatigue, malaise, weak, aching, decreased app
hallmark s/s is fever, except for older pt and immunosuppressed pt

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28
Q

aplastic anemia

A

bone marrow suppression leads to decreased production of RBC (toxic, radiation, immune injury)

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29
Q

anemia of chronic disease

A

chronic infection, inflammation, malignancy leads to increased demand or suppression of RBC

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30
Q

folate deficiency (B vit)

A

lack of folate leads to premature cell death

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31
Q

Iron deficiency

A

most common cause of anemia and most common nut deficiency in the world
lack of iron leads to lack of hemoglobin

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32
Q

thalassemia

A

impaired synthesis of hemoglobin chain; congenital

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33
Q

sickle cell anemia

A

abnormal hemoglobin molecule (don’t have same o2 carrying ability); congenital

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34
Q

hemolytic disease of newborn

A

maternal antibodies cause destruction of fetal cells

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35
Q

acute blood loss

as related to type of anemia

A

blood loss leads to insufficient RBC

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36
Q

pernicious anemia

A

lack of vit B leads to altered DNA synth

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37
Q 
post hemorrhage 
(as related to type of anemia)
A

blood loss leads to insufficient RBC

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38
Q

erythropoiesis

A

hormone secreted by kidney in response to cellular hypoxia; stimulates RBC production in bone marrow

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39
Q

claudication

A

pain in muscle

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40
Q

DPG

A

type of salt in cell’s protein- helps hgb release o2 easier (more DPG = more o2)

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41
Q

cardiac output

A

volume of blood output from heart per min; made up of two components: CO = HR x SV

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42
Q

Stroke volume (SV)

A

volume of blood pumped out of the left ventricle with every heart beat

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43
Q

mild symptoms of anemia

A

none; compensatory mechanisms are working

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44
Q

moderate symptoms of anemia

A

fatigue, malaise, loss of E, tachycardia, exertional dyspnea

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45
Q

mod to severe symptoms of anemia

A

orthostatic/general hypotension; vasoconstriction->pallor; tachypnea/dyspnea; tachycardia/transient murmur, angina pectoris; intermittent claudication; night cramps in muscles; h/a, light headedness, faintness; tinnitus (noise/ringing in ears)

46
Q

relative v absolute anemia

A

relative: increase in total RBC mass with an increase in plasma vol (which causes decreased hgb content in bl…diluted); ie: pregnancy
absolute: decrease in number of RBC

47
Q

microcytic anemia

A

type of iron def anemia (secondary to…); presence of hypochromic RBC in bl smear

48
Q

Hypochromic anemia

A

generic term for any type of anemia in which the RBC are paler than normal. (Hypo- less, chromic-color.) A normal red blood cell will have an area of pallor in the center of it

49
Q

etiology of iron deficiency anemia

A

1 decreased absorption (bc of body’s ability/chronic illness)
2 physiologic increase in general requirement (pregnancy)
3 excessive iron loss (normal bl loss)
4 renal issues

50
Q

hemostasis

A

physical process that stops bleeding @ site of injury while maintaining norm bl flow elsewhere

51
Q

primary hemostasis

A

interaction between platelets and the endothelium of the injured blood vessel; immediate response to trauma is vasoconstriction to reduce blood loss, resulting from vasospasm; then forms “platelet plug” that adheres and clumps in 3-7m

52
Q

secondary hemostasis

A

involves formation of fibrin clot (coagulation) to maintain primary hemostasis efforts; happens via intrinsic/extrinsic pathways and is series of clotting factors being activated (fibrinogen to fibrin) over 3-10m; final stage: clot retraction (firm clot formed) by 1h

53
Q

key players in hemostasis

always in body; part of both primary and 2ndary hemostasis

A
  • platelets (thrombocytes): activators coagulation factors; degranulation triggers the cascade effect; stickiness helps them adhere to endothelium and each other (clump together)
  • coagulation factors: activated by platelets, and then activate each other or tissue factors; mostly plasma proteins produced by the liver that are normally circulating in the blood
54
Q

prothrombin (PTR) & INR lab tests

A

evaluate extrinsic pathway of coagulation

55
Q

activated partial thromboplastin time (aPTI) lab test

A

evaluate intrinsic pathway of coagulation

56
Q

Virchow’s triad

A

(risks for thrombus)

  • circulatory stasis: (immobile/laying for period of time)
  • hypercoaguable condition: body pushed towards increased coagulation ie: pregnancy, oral contra, chemo/cancer pt, obesity
  • endothelial/vessel wall injury: trauma ie: IV, cath, smoking, hypertension
  • *C-s pt meets all these criteria!
57
Q

blood pressure equation

A

BP = CO (bl vol output/min) x SVR (resistance overcome to push bl thru circ system & create flow)

58
Q

edema/hypervolemia

A

excessive accumulation of fluid w/in the interstitial space

59
Q

forces involved in edema/hypervolemia

A

1 increased capillary hydrostatic pressure
2 increased interstitial oncotic pressure
3 increased cap membrane permeability
4 lymphatic channel obstruction (can’t carry waste away)

60
Q

clinical dehydration/hypovolemia

A

too small volume of fluid in the extracellular space (vascular/plasma/interstitial); body fluids are too concentrated

61
Q

forces involved in dehydration/hypovolemia

A

1 fluid loss: emesis, hemorrhage, diarrhea, polyuria, diaphoresis
2 reduced fluid intake: GI issues/altered mental status
3 fluid shift: burns…edema in some spaces but not the right ones (interstitial space)

62
Q

Na

A 
135-145 mEq/L
major ECF cation
nerve conduction & neuromuscular fct
regulates acid-base balance
maintains water balance
63
Q

clinical manifestations of hyponatremia

A

CNS dysfunction:
confusion/lethargy…seizures/coma
n/v, h/a

64
Q

clinical manifestations of hypernatremia

A 
(increased conc of fluid = dehydration)...
thirst/dry mucuous membranes
hypotension
tachycardia
oliguria
confusion/lethargy...seizures/coma
65
Q

Potassium

A 
3.5-5 mEq/L
major ICF cation
cardiac muscle contractions
maintains acid-base balance
neuromuscular transm of nerve impulses
*heart and GI
66
Q

clinical manifestations of hypokalemia

A
  • smooth and skeletal muscles HYPERpolarized (less reactive to stimuli); ie: GI- abdominal dissension, decreased bowels/paralytic ileum; general muscle weakness
  • cardiac: dysrhythmias
67
Q

clinical manifestations of hyperkalemia

A
  • smooth and skeletal muscles HYPOpolarized- can’t fire again after discharge; GI cramping/diarrhea; general muscle weakness
  • cardiac: dysrhythmias/cardiac arrest
  • dialysis if kidneys not functioning
68
Q

Calcium

A 
9-11 mg; 4.5-5.5 mEq/L
heart protectant- cardiac AP
CNS- nerve impulse transm
bone, teeth, muscle contraction
blood coagulation
69
Q

clinical manifestations of hypocalcemia

A

increased neuromuscular excitabilit/hyperactive reflexes: twitching, seizures, tetany
heart dysrhythmias

70
Q

clinical manifestations of hypercalcemia

A

decreased neuromuscular excitability/diminished reflexes: weakness, paralysis, constipation
CNS: fatigue, lethargy, confusion
n/v
heart dysrhythmias- heart block, bradycardia
kidney stones

71
Q

3 major mechanisms regulating acid-base status

A 
Bicarbonate-carbonic acid buffer system (ECF; always happening in body); 20 HCO3: 1 CO2; *body adjusts carbonic acid to maintain pH ratio
respiratory system (2nd line- fast acting)
renal system (2nd line- slow acting)
72
Q

respiratory acidosis

A

condition that causes excess carbonic acid (aka you’re shallow breathing/not taking deep breaths)…
- impaired gas exchange: asthma, COPD, pneumonia
- inadequate neuromuscular fct: injury, surgery, pain
- impairment of respiratory control in the brainstem: opioids
ABG’s: increased co2 and decreased pH

73
Q

clinical manifestations of respiratory acidosis

A

neuro: blurred vision, tremors
h/a, lethargy
tachycardia, heart dysrhythmias

74
Q

respiratory alkalosis

A

condition that causes a carbonic acid deficit: hyperventilation– panic attack, anxiety, crying (peds), acute pain, hypoxemia, brain stem injury
ABG’s: decreased CO2 and increased pH

75
Q

clinical manifestations of respiratory alkalosis

A

increased neuromuscular excitability- numbness, tingling, spasms
excitation/confusion
cerebral vasoconstriction

76
Q

Metabolic acidosis

A

excess of any acid except carbonic acid
- increase in metabolic acid (diabetic ketoacidosis (type I), burns, shock
- decrease in base (bicarb): severe diarrhea, intestinal decompression
- combo of both
ABG’s: decreased HCO3 and decreased pH

77
Q

clinical manifestations of metabolic acidosis

A

fruity breath
GI: n/v, diarrhea–>dehydration
CNS dep: h/a, confusion, lethargy, coma
cardiac: tachycardia, dysrhythmia

78
Q

metabolic alkalosis

A

deficit of any acid except carbonic acid
- increase in base: overuse antacids, hypovolemic
- decrease in acid: emesis, gastric secretion removal (tube)
- combo of both (hypokalemia…diuretics)
ABG’s: increase in HCO3 and increase in pH

79
Q

clinical manifestations of metabolic alkalosis

A

CNS irritability, and then depression: tingling, tetany, seizures
ECF vol depletion: n/v, diarrhea, hypotension
hypokalemia w/ muscle weakness

80
Q

bacterial enzyme

A

helps organism exist in environment

81
Q

antiphagocytic factors

A

microbes containing outside coding that leave them unrecognizable to body’s phagocytic defense mechanisms (leukocytes)
also help w/ adherence

82
Q

mode of transmission

A

droplet, airborne, oral/fecal, vector

83
Q

vector

A

any get that carries/transmits an infectious pathogen into another living organism

84
Q

negative intraplural pressure

A

produced by babies (coughing/crying) to open collapsed alveoli after birth

85
Q

importance of surfactant

A

decreases the surface tension of alveolar fluids and helps alveoli open more easily after birth

86
Q

reasons of closure for…
foramen ovale
ductus arteriosus
ductus venosus

A
  • pressure change in atria
  • increased oxygen of blood
  • unsure
87
Q

-plasia

A

growth & dev (mitotic division)

ie: increased altitude–> body produces more RBC

88
Q

mechanism of lack of o2 in body

A 
atp pro in cell ceases
ATP dependent pumps fail
Na accumulates in cell-> cell swells
excess calcium interferes
glycogen depleted
lactic acid produced
pH decreases...causes dysfunction
89
Q

reperfusion injury

A
  • calcium overload (when we reperfuse body is washed w ca
  • formation of reactive o species
  • *both can trigger apoptosis
  • inflammation
90
Q

mycoses/mycotic infection

A

any disease/infection caused by fungi

91
Q

chain of infection

A 
agent
resevoir
portal of entry/exit
mode of trans
portal of exit/entry
host
92
Q

pica

A

craving of non-food substances; can occur w/ iron deficiency anemia

93
Q

vascular purpura

A

disease causing swelling/inflammation of bl vessels (vasculitis)
when bl vessels bleed you get the purpura rash

94
Q

normal platelet count

A

200k-400k

<100k? hemorrhage concern…bl can’t clot…can’t admin pitocin

95
Q

types of coagulation disorders

deficiencies of one or more clotting factors

A
  • vit k def…admin supp
  • inherited: Von Willebrand- lack of glycoprotein in bl, causing inability to clot; hemophelia- bl can’t clot normally
  • disseminated intravascular coagulation (DIC)- late stage of HELLP
96
Q

hemarthrosis

A

blood in joints

97
Q

hematoma

A

blood in brain

98
Q

petechia

A

capillary hemorrhages;

*purpura are groups/patches of peticha

99
Q

hemtochezia

A

blood in stool

100
Q

hemoprysis

A

blood in sputum

101
Q

intrinsic v extrinsic pathway of coag cascade

A

intrinsic is triggered when bl comes into contact w/ endothelium…platelets forming
extrinsic triggered by tissue factor (trauma)
*both pathways come down to common pathway and activate factor X….which activates Xa

102
Q

treatment of bleeding discorders

A
  • avoid cause (from a med? stop the med!)
  • steroids- stimulates immune response- prevents breakdown of platelets
  • admin IVIG - intravenous immunoglobulin…prevents bleeding (in the short term - days/weeks)
  • factor replacement (whichever needed)
  • admin plasma/platelet
103
Q

thrombocytopenia

A

decreased pro or increased demand of platelets

assess: petechiae, purpura, bleeding, decreased platelet count in lab
treat: treat/remove root of cause; block imm response; bl/platelet transfusion

104
Q

deep vein thrombosis

A

i. d.: ultrasound or labs->d dimer (neg= don’t have)

treat: thrombolytic (tPA) med to break down clot; anticoagulant to prevent further clotting

105
Q

estrogen (as related to UTI)

A

the urethra is an estrogen dependent structure; lack of estrogen = more prone to infection; lack of estrogen–> prepubescent/post menopause

106
Q

uropathogenic properties (pathogens causing UTIs)

A
  • ability to attach to uroepithelial cells (fimbriae/pilli)
  • ability to attach to latex cath
  • ability to express toxins
  • ability to produce biofilms (harder to breakdown/eradicate)
107
Q

most common uropathogens

A 
e coli
STIs
pseudomonas
staph sprophyticus
klebisella
proteus
108
Q

PID

A

infection of cervix (cervicitis), ovaries (oophoritis), uterus (endometritis), oviducts (salpingitis)
aerobic & anaerobic
gonorrhea and chlamydia most common

109
Q

mechanisms behind preeclampsia

A

maternal immunologic intolerance
abnormal placental implantation
CV/inflamm changes

110
Q

labs to draw for hypertensive disease in pregnancy

A

protein in urine
liver enzymes
platelet count (low= thrombocytopenia–>hemorrhage)

398 pharm/patho (2 decks)

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