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Spring A 2025 > patho exam 1 > Flashcards

patho exam 1 Flashcards

1
Q

urinary system

A

two kidneys
two ureters
urinary bladder
urethra

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2
Q

where do the kidneys lie?

A

on the rear wall of abdomen
T12-L3 level

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3
Q

how much cardiac output do the kidneys receive?

A

20%

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4
Q

what are the primary functions of the kidneys?

A

filter blood and produce urine
regulation of plasma ionic composition
regulation of plasma volume
regulation of plasma osmolarity
regulation of plasma hydrogen ion concentration

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5
Q

what are the secondary functions of the kidney?

A

secrete erythropoietin
secrete renin
activate vitamin D3

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6
Q

what does a nephron consist of?

A

renal corpuscles
renal tubule

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7
Q

superficial/cortical nephron

A

entirely within cortex

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8
Q

juxtamedullary nephron

A

15-20% of all

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9
Q

what is the first step in formation of urine?

A

glomerular filtration

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10
Q

names for the fluid that is filtered

A

filtrate
glomerular filtrate
ultrafiltrate

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11
Q

what does filtrate consist of?

A

water and small solutes

does not have:
blood cells and proteins

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12
Q

what are the starling forces

A

two hydrostatic and two oncotic pressures

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13
Q

what forces favor filtration?

A

glomerular HP
bowman’s OP

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14
Q

what forces oppose filtration?

A

bowman’s HP
glomerular OP

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15
Q

what is oncotic pressure?

A

pressure due to the presence of proteins in the blood

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16
Q

what GFR is considered kidney failure?

A

less than 15%

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17
Q

filtration

A

bulk flow of protein free plasma from glom capillaries into bowman’s capsule

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18
Q

reabsorption

A

water and solutes reabsorbed from glomular filtrate into peritubular capillary

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19
Q

secretion

A

net result of processes of filtration, reabsorption and secretion

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20
Q

normal values for routine urinalysis

A

color - yellow amber
appearance - clear to slightly hazy
volume - 600-2500ml/24 hrs
glucose - neg
ketones - neg
protein - neg
RBC - neg
WBC - neg

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21
Q

GFR (glomular filtration rate)

A

very timed manner of collecting blood and urine
now using estimated GFR

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22
Q

serum creatinine

A

waste product of muscle metabolism
if SC doubles, GFR has fallen to 1/2

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23
Q

blood urea nitrogen

A

end product of protein metabolism
indicator of liver and kidney function
2/3rd renal function lost before sig rise

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24
Q

possible etiologies with proteinuria

A

renal failure
nephrotic syndrome preeclampsia
renal artery/vein thrombosis
glomerular disease
tubulopathy

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25
Q

possible etiologies with glucosuria

A

diabetes mellitus

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26
Q

possible etiologies with ketonuria

A

diabetes mellitus
ketoacidosis
starvation

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27
Q

possible etiologies with hematuria

A

glomerular damage
tumors
kidney trauma
urinary tract infection
acute tubular necrosis
urinary tract obstruction

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28
Q

possible etiologies with pyuria

A

upper and lower urinary tract infection
acute golmerulonephritis
renal calculi

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29
Q

possible etiologies with bacteruria

A

upper and lower urinary tract infection

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30
Q

polycystic kidney disease

A

fluid filled sacs
single or multiple
progressive
inherited or acquired

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31
Q

autosomal dominant polycystic kidney disease

A

account for 10% of ESRD, 4th leading cause
thousands of fluid sacs
slow progression
kidneys enlarged and misshapen
most common PKD

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32
Q

manifestations of ADPKD

A

pain
infected cysts
hematuria
enlarged kidneys
hypertension
headaches, nauseam vomiting
hemorrhages

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33
Q

autosomal recessive polycystic kidney disease

A

1 in 20,000 live births
mutation in PKHD1
evident at birth
restricts lung development
10 year survival rate beyond 1 year of life

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34
Q

glomerulonephritis

A

affects men more than women
leading cause of chronic kidney disease
nephritic vs nephrotic

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35
Q

nephrotic syndrome

A

inflammation occludes glom capillary lumen

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36
Q

clinical findings of nephrotic syndrome

A

massive proteinuria
hypoalbuminemia
generalized edema
dyspnea
hyperlipidemia
lipiduria
dark, cloudy urine

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37
Q

nephritic syndrome

A

circulating immune complexes become trapped in glomerular membrane

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38
Q

clinical manifestations of nephritic syndrome

A

hematuria
proteinuria
low GFR
azotemia
oliguria
hypertension

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39
Q

treatment of glomerulonephritis

A

antibiotics
corticosteroids
blood pressure management
temporary dialysis

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40
Q

chronic kidney disease

A

1 in 9 adults
gradual irreversible loss of renal function
3+ months
unable to regulate fluid and electrolytes
GFR less than 60ml/min

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41
Q

most common causes of CKD

A

diabetes mellitus
hypertension
glomerulonephritis
PKD

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42
Q

stage 1 kidney failure

A

no overt symptoms
unaffected nephrons hypertrophy
hypertension and anemia

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43
Q

stage 2 kidney failure

A

small amount of albumin is excreted in urine

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44
Q

stage 3 kidney disease

A

albumin levels increase in urine and decrease in blood
increase of waste in blood - azotemia

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45
Q

stage 4 and 5 kidney failure

A

complications appear
proteinuria
hypertensive

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46
Q

stage 5 kidney failure

A

cannot excrete toxins
uremia
all systems affected

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47
Q

red flags of CKD

A

recurrent infections
edema
numbness
trouble breathing
ulcerations
heart failure
platelet dysfunction
hypertension
memory loss
seizures
renal osteodystrophy

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48
Q

clinical manifestations of kidney failure

A

tired, weak, pale skin
itchy, dry skin, less sweating
metallic taste
hypertension
platelet dysfunction
anorexia, nausea
electrolyte imbalances
respiratory distress
infections
memory loss
osteodystrophy

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49
Q

diagnosis of CKD

A

initial symptoms are vague
tests: CBC, BUN, CT, MRI

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50
Q

treatment of kidney failure

A

prevention: control diabetes, hypertension
treat underlying disease
protein restriction
adequate fat and carbs
potassium restriction
remain hydrated
dialysis
transplant

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51
Q

hemodialysis

A

in clinic
cleanses the blood

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52
Q

peritoneal dialysis

A

can be done at home
ambulatory: 4 times a day
cycle assisted: machine, during sleep, 7-10 hrs

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53
Q

precautions when on dialysis

A

keep dialysis site clean and dry
staying properly hydrated
avoid overexertion
staying aware of cognitive and physical state
preferred when dialysis not running

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54
Q

red flags when on dialysis

A

acute infection or fever
hypotension
chest pain or SOA
bleeding at dialysis site
abnormal hearth rhythms
decreased consciousness

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55
Q

kidney transplant

A

primary indication is T1D with ESRD
younger than 45
less expensive than LT dialysis

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56
Q

5 year survival rate for pancreas-kidney transplant

A

95%

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57
Q

5 year survival rate for kidney transplant

A

88%

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58
Q

PT and CKD

A

high risk of CVD
PT helps manage symptoms and manifestations
suggest to burn 1000 Kcal a week

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59
Q

barriers/contraindications to PT with CKD

A

previous experiences with exercise
time
sick role - may exacerbate, accepting fate
pain/fatigue/lethargy
motivation
post op recovery
uncontrolled CVD, DM
infection

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60
Q

recommendations for PT with CKD

A

30 min 3-5x/week
muscle strengthening, flexibility, balance
increase difficulty
cardiovascular - biking

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61
Q

dialysis is best when combines with what?

A

aerobic and resistance exercise

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62
Q

what to look out for when working with dialysis pts?

A

depression
lack of motivation
calling in to therapy
weakness, fatigue
tachycardia, dizziness, nausea

schedule before dialysis or on day off
monitor vitals before, during and after

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63
Q

define pathophysiology

A

study of functional changes that occur in the body as a result of the mechanism of disease

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64
Q

define pathogenesis

A

development of cellular events and reactions,
development of the disease

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65
Q

what does the cell membrane do?

A

protection
selective permeable - decides what goes in and out

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66
Q

function of nucleus

A

control center

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67
Q

function of nucleolus

A

produces RNA

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68
Q

function of endoplasmic reticulum

A

synthesizes enzymes and proteins

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69
Q

function of ribosomes

A

aid in protein protection

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70
Q

function of golgi proteins

A

sorts, modifies, and packages proteins

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71
Q

function of lysosomes

A

digests waste

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72
Q

function of mitochondria

A

produces ATP

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73
Q

where is epithelial tissue found?

A

outer surface of body
lines GI
lines respiratory
lines blood vessels

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74
Q

functions of epithelial tissues

A

barrier, protection
absorption
filtration
secretion
permeability
regeneration

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75
Q

3 types of epithelial tissues

A

squamous: thin and flat
cuboidal: cube shape
columnar

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76
Q

location of cuboidal cells

A

surface of ovary and thyroid

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77
Q

location of columnar cells

A

lines intestines

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78
Q

3 ways to describe layers of epithelial cells

A

simple: one layer
stratified: multiple layers
pseudostratified: looks like multiple but actually one

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79
Q

location of three types of simple epithelial cells

A

Sim squam: lines blood vessels, lymph nodes, alveoli
Sim cub: glands
Sim col: digestive tract

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80
Q

location of three types of stratified epithelial cells

A

Strat squam: skin
Strat cub: sweat and salivary glands
Strat col: (VERY RARE) conjunctiva

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81
Q

pseudostratified epithelial tissue

A

all cells in contact with underlying matrix
not all extend to surface
P col: most of upper respiratory tract

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82
Q

transitional epithelium

A

can change shape when stretched
ex: urinary bladder, urethra, ureters

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83
Q

components of connective tissue

A

cells
extracellular protein fibers
ground substance

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84
Q

examples of connective tissue

A

tendons
ligaments
adipose tissue
cartilage
bone
blood and lymph

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85
Q

marfan syndrome

A

CT disorder
1 in 5,000 people

damages blood vessels, hearts, eyes skin, lungs, and bones
tall slender build
flat feet
aortic aneurysm common

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86
Q

describe skeletal muscle

A

long and cylindrical
striated
voluntary

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87
Q

describe smooth muscle

A

visceral organs
nonstriated
spindle shape
invol
intercalated disks/gap junctions

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88
Q

describe cardiac muscle

A

shorter, branched
invol
striated
intercalated disks/gap junctions

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89
Q

skeletal muscle layers (inside to out)

A

endomysium
perimysium
epimysium

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90
Q

describe the three troponins

A

T - attaches troponin to tropomyosin
I - inhibits interaction between actin and myosin
C - calcium binding protein

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91
Q

function of transverse tubules

A

action potential travels through

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92
Q

function of sarcoplasmic reticulum

A

around myofibrils
accumulates calcium
keeps intercellular calcium concentration low when at rest

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93
Q

steps in excitation contraction coupling

A

action potential to t tubule
depolarization of t tubule
open SR calcium release channels
increase intracellular calcium concentration
calcium bind to troponin C
tropomyosin moves and allows interaction of actin and myosin
cross-bridge cycling
contraction/force generation

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94
Q

steps in cross bridge cycle

A

ATP binds to myosin head, myosin released
myosin head displaced forward, ATP hydrolysis into ADP and Pi
myosin head binds to new site on actin, power stroke
ADP released, rigor

AKA sliding filament theory

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95
Q

length-tension relationship

A

need just enough overlap but not 100% shortened or lengthened

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96
Q

facts about cardiac muscle

A

muscle cells - cardiomyocytes
increase in troponin is used to diagnose heart attack

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97
Q

facts about smooth muscle

A

invol
lacks striations
found in walls of hollow organs
produces motility
maintains tension
calcium binding protein called calmodulin

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98
Q

which portion of sarcomere’s length remains same during excitation contraction coupling?

A

A band

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99
Q

which is not related?

skeletal
striated
visceral
voluntary

A

visceral

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100
Q

which is not related?

smooth
visceral
voluntary
organs

A

voluntary

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101
Q

which is not related?

cardiac
branching
visceral
involuntary

A

visceral

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102
Q

define reversible cell injury

A

cell is able to recover homeostasis after removal of stress

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103
Q

atrophy

A

decreased cell size

causes: disuse, denervation

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104
Q

cerebral atrophy

A

reduction of size of brain cells in cerebrum

causes: TBI, infections

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105
Q

hypertrophy

A

increased cell size
seen in cardiac and skeletal muscle

causes: increase workload, increased hormones

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106
Q

hyperplasia

A

increased cell number
seen in epidermis, intestinal epithelium

cause: hormonal signaling and increase in work load

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107
Q

metaplasia

A

conversion of one cell type to another

cause: irritation, inflammation
cigarette smoker
GERD

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108
Q

dysplasia

A

disorderly growth
precursor of cancer

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109
Q

what if the cells do not have the ability to adapt to stressors?

A

cell death

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110
Q

irreversible cell injury

A

alterations in cell nucleus
rupture of cell membrane
release of digestive enzymes
release contents to ECF

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111
Q

reversible cell injury

A

swelling
membrane blebs

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112
Q

define necrosis

A

damaged cells
initiates inflammation

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113
Q

define apoptosis

A

programmed cell death
does not initiate inflammation

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114
Q

3 lines of defense for immunity

A

skin and mucous membrane
inflammation
immunity

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115
Q

function of neutrophil

A

inflammation
defense against foreign substances like bacteria, fungi

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116
Q

function of monocytes

A

immature macrophages
clean up debris/damaged cells

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117
Q

eosinophils

A

attack parasites, cancer cells
play a role in asthma and allergy

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118
Q

basophils

A

produce allergic response like sneezing

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119
Q

lymphocytes (T and B)

A

immunity
produce antibodies
kills antigens

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120
Q

purpose of inflammation

A

essential to healing
paves to way for repair of injured tissue

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121
Q

acute inflammation

A

expected response to injury
restoration of tissue homeostasis

vascular and cellular phase

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122
Q

chronic inflammation

A

days to years
unrelenting injury
cells involved: monocytes, macrophages, fibroblasts
only have symptoms during flare ups

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123
Q

cardinal signs of inflammation

A

rubor (redness)
tumor (swelling)
calor (heat)
dolor (pain)
functio lasea (loss of function)

systematic manifestations: fever, leukocytosis

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124
Q

vascular phase

A

marked by tissue edema
constriction followed by dilation
increased permeability
swelling, pain, impaired function

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125
Q

cellular phase

A

chemotaxis
adhesion to endothelium
transmigration across endothelium

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126
Q

what cells are active in cellular phase?

A

WBC
RBC
platelets
CT cells
ECM - elastin, collagen

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127
Q

what mediators cause vasodilation

A

prostaglandins
histamine
nitric oxide

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128
Q

what mediators cause vascular permeability

A

histamine
bradykinin
leukotrienes
PAF

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129
Q

what mediators cause pain

A

prostaglandins
bradykinins

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130
Q

what mediators cause fever

A

prostaglandins

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131
Q

what mediators cause leukocytosis

A

leukocytes
mast cells and eosinophils
granulocytes
monocytes
natural killer cells

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132
Q

what mediators limit inflammation

A

histaminase
kinases

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133
Q

what mediators repair and heal

A

TGF -B
angiogenic factors

134
Q

what mediators cause phagocytosis

A

leukotrienes

135
Q

how does WBC change with inflammation?

A

increase

136
Q

how does c-reactive protein change with inflammation?

A

increase

137
Q

how does prothrombin (time to coagulate) change with inflammation?

A

reduced

coag faster

138
Q

how does fibrinogen change with inflammation?

A

increased

needed for fibrin to cause clotting

139
Q

how does WBC differential change with inflammation?

A

neutrophils increase in acute inflammation

140
Q

how does ESR change with inflammation?

A

increase often above 100mm/hr

erythrocyte sedimentation rate - how fast blood samples sediments in a tube in an hour
nonspecific

141
Q

CRP

A

synthesized in liver
nonspecific, but more accurate than ESR

142
Q

sequence of cell injury

A

irritant enters
cell damage
inflammatory mediators
blood vessels dilate
redness, heat, edema
WBC migrate
phagocytosis

143
Q

two ways of tissue repair

A

regeneration: injured cells replaces with healthy
replacement with CT (scar)

144
Q

phases of wound healing

A

inflammation - 5-10 days
proliferation and migration - 3-20 days
remodeling and maturation - past 21 days

145
Q

components of tissue healing

A

fibronectin - helps with blood clot
proteoglycans - hydration
elastin
collagen - support and tensile strength

146
Q

factors that affect tissue healing

A

growth factors - VEG-F, fibroblasts form new blood cells
general health of individual
presence of comorbidities
infection
off loading weight bearing surfaces may be necessary
lack of desire to exercise or follow plan or care
nutrition - iron, vit A and C, arginine, high protein intake
oxygen

147
Q

arginine

A

enhances healing and immune function

148
Q

migration of phagocytic white blood cells into injured area: what comes next?

A

neutrophils come first to remove bacteria
macrophages in 24 hrs
release growth factors for proliferative stage
form granulation tissue

149
Q

angiogenesis

A

formation of new blood vessels

150
Q

granulation tissue

A

reddish granular layer of tissue

151
Q

re-epithelialization

A

proliferate to form new surface layer
filling in gap in the wound
makes a scab

152
Q

remodeling phase

A

3 weeks after injury
red to pink to white

153
Q

factors that impact wound healing

A

inflammatory/immune response
inadequate nutritional status
poor tissue perfusion

154
Q

complications of wound healing and tissue repair

A

infection
ulceration
adhesions
dehiscence (wounds pull apart)
keloid development

155
Q

wound healing continuum colors

A

black- dead
yellow- infection
red- healing in granulation phase
pink- healing, re-epi

156
Q

what is a granuloma?

A

form chronic inflammation
when injury is too difficult to control
lymphocytes attempt to surround foreign body

157
Q

difference between time in acute and chronic inflammation

A

acute: resolution within a few weeks
chronic: present for prolonged period of time

158
Q

difference between chief phagocytic cells in acute and chronic inflammation

A

acute: neutrophils
chronic: monocytes, macrophages

159
Q

difference between restoration in acute and chronic inflammation

A

acute: minimal scarring
chronic: marked by fibrosis, scarring or granulation

160
Q

you get a papercut and experience pain at the site. this response is related to:

A

increases exudate and chemical mediators at the site

161
Q

antigens

A

any foreign substance that elicits an immune response

162
Q

antibody

A

responds to antigens

163
Q

innate immunity

A

born with it
1st reponder
rapid and always the same
nonspecific
non adaptive

164
Q

acquired/adaptive immunity

A

slower response
diverse
specific
has memory
self and non self recognition

165
Q

active acquired immunity

A

get sick
vaccine

166
Q

passive acquired immunity

A

transferred from person to person

ex: mother to fetus

167
Q

two types of cells in adaptive/acquired immunity

A

humoral - B
cell mediated - T

168
Q

how to B and T cells move through the body?

A

migrate through blood, lymph and lymph nodes

169
Q

humoral immunity

A

involves antibodies/immunoglobulins
B cells originate and mature in bone marrow

170
Q

cell mediated immunity

A

cannot be passively transferred
originate in bone marrow and mature in thymus
recognize hidden organisms
helper T cells are called CD4
cytotoxic T cells called CD8
suppressor T cells
memory T cells

171
Q

factors altering the immune system

A

aging
nutrition - vit A and E, zinc
burns - decrease neutrophil function
sleep disturbances
illness and disease
drugs
surgery/anesthesia

172
Q

exercise immunology

A

mod intensity enhances immune function
neut, NK, lymphocytes all increase

173
Q

immune system disorders

A

primary: defect involving cells
secondary: results from an underlying disease/factor

174
Q

AIDS

A

first recognized in 1981, HIV in 1986
infects CD4, dendritic, macrophages
progressive destruction of T cells
immunodeficiency

175
Q

pathophysiology of AIDS

A

transmitted through bodily fluids
risk factors include: poverty, drugs, bad health care

176
Q

pathogenesis of AIDS

A

retrovirus
attacks and inactivates CD4
high mutation rate
continual destruction of CD4
progressive loss immune function

177
Q

steps to pathogenesis of AIDS

A

binding of virus to CD4
enter host cells
reverse transcription
integrate into host DNA and replicate
transcription
translation
assembly of HIV proteins
budding and release new virion
HIV replication

178
Q

HIV spectrum

A

asymptomatic: CD4 count >500
symptomatic: CD4 count 200-500
advanced: <200

normal is 600-1200

179
Q

clinical manifestation of HIV

A

acute: 1-6 weeks after exposure
asymp: positive for antibodies, 1-20 years
symp: nonspecific symptoms, progresses to HIV
advanced: neuro involvement, opportunistic infections

pain syndromes
high calorie, high protein diet
lipodystrophy - defective fat metabolism

180
Q

dermatologic conditions of AIDS

A

hair loss
rash
delayed wound healing
dry flaking skin
kaposi sarcoma - purple cancer

181
Q

diagnosis of HIV/AIDS

A

screening in individuals aged 13-64 yrs
blood tests or oral fluid

182
Q

treatment for HIV/AIDS

A

no cure
HAART - highly active antiretroviral therapy
NSAIDS and pain meds
possible vaccines in the future

183
Q

entry inhibitors

A

block HIV from connecting to CD4

184
Q

nukes and non nukes

A

stop HIV changing from RNA to DNA

185
Q

integrase inhibitors

A

block HIV from being integrates into cell’s DNA

186
Q

protease inhibitors

A

block new HIV from being cut into smaller proteins

187
Q

special implications for the therapist (HIV/AIDS)

A

women victim of domestic violence
msk or neuro problems with unknown origin

188
Q

exercise and HIV

A

moderate is good
strenuous is bad

management of physical dysfunctions
regular exercise encouraged
address impairment
monitor response to exercise
avoid overtraining

189
Q

post exposure prophylaxis

A

call CDC
28 days course of HAART
avoid spreading your fluids

190
Q

hypersensitivity type 1

A

IgE mediated
most common
immediate
severe - anaphylactic shock

191
Q

hypersensitivity type 2

A

IgG, IgM mediated
antibody mediated
basis of autoimmune disease

192
Q

hypersensitivity type 3

A

IgG, IgM, complement mediated
formation of antigen-antibody immune complexes
massive inflammatory response

193
Q

hypersensitivity type 4

A

T cell mediated
delayed
transplant rejection

194
Q

autoimmune disorders (hypersensitivity type 2)

A

addison’s
crohn’s
T1D
polymyositis/dermatomyositis
thyroiditis
ulcerative colitis
MS
MG
RA

195
Q

systemic lupus erythematosus

A

type 2 reaction
inflammation wherever antibody complex deposits
common in women
butterfly rash on nose and cheeks
affects kidneys and MSK
treatment: NSAIDs and corticosteroids

196
Q

facts about blood

A

is CT
has cells suspended in liquid matrix
5 liters in the body
7-8% of total body weight

197
Q

blood composition: overview

A

plasma - 55%
red blood cells
platelets
white blood cells

198
Q

components of plasma

A

proteins - 7%
water - 91.5%
other solutes - 2%

199
Q

what proteins are in blood?

A

albumin - 54%
fibrinogen - 7%
globulins - 38%
others - 1%

200
Q

what “other solutes” are present in blood?

A

electrolytes
hormones, enzymes
nutrients, carbohydrates, fats
gases
waste products

201
Q

what is the function of plasma?

A

transport nutrients, chemical messengers and metabolites

202
Q

what is the function of albumin?

A

maintains plasma oncotic pressure
maintains blood volume
serves as a carrier

203
Q

what is the function of globulins?

A

alpha - transports bilirubin
beta - transports iron
gamma - anitbodies of immune system

204
Q

what is the function of fibrinogen?

A

helps form fibrin for clotting

205
Q

plasma vs serum

A

plasma - treated with anti-coagulants
serum - liquid after coagulation

206
Q

facts about red blood cells

A

most common blood cells
transport oxygen to tissues and co2 out of tissues
each hemoglobin carries for oxygens
productions in bone marrow

207
Q

what is the life span of RBCs

A

about 120 days
iron is recycles in small intestine after cell death

globin is recycled
heme turns to bilirubin and is excreted

208
Q

hematocrit

A

percent of RBCs in blood
women: 37-47
men: 42-52
anemia - not enough
polycythemia - excess

209
Q

anemia

A

common
abnormally low RBCs

210
Q

causes of anemia

A

blood loss
destruction
inadequate or defective RBC production
reduction in hemoglobin content
abnormal hemoglobin

211
Q

general features of anemia

A

weakness
fatigue
dyspnea
hypoxia of brain tissue
pallor - absence of red
tachycardia
severe - heart failure
increased respiration rate
bone pain

212
Q

3 types of anemia

A

iron deficiency
megaloblastic
sickle cell disease

213
Q

iron deficiency anemia (definition and causes)

A

iron does not meet demands of hemoglobin production

causes:
decreased iron consumption
increased iron demand

214
Q

where is iron stored?

A

ferritin
transferrin

215
Q

what groups are at risk for iron deficiency anemia?

A

pregnant women
women with heavy menstrual bleeding
infants and younger children
frequent blood donors
cancer, GI, surgical pts
vegetarian diet

216
Q

features of iron deficiency anemia

A

fatigue
brittle nails
headache
delayed healing
tachycardia
decreased appetite
unusual food cravings
neuro impairment or damage

217
Q

IDA diagnosis

A

low hemoglobin and hematocrit
RBCs microcytic and hypochromic
serum ferritin
serum iron

218
Q

IDA treatment

A

treating cause
consuming iron rich foods
iron supplements
high vitamin c for absorption

219
Q

megaloblastic anemia (definition and causes)

A

impaired DNA synthesis - large immature RBCs

causes:
B12 deficiency - decreased cell division & maturation
folic acid deficiency

220
Q

megaloblastic - pernicious anemia

A

absence of intrinsic factors in stomach
inhibits absorption of B12

221
Q

features of megaloblastic anemia

A

bleeding gums
diarrhea
anorexia
demyelination
paresthesia of hands and feet
impaired sense of smell
personality/memory changes
mild jaundice

222
Q

diagnosis of megaloblastic anemia

A

serum vitamin B12
CBC
IF antibodies
RBCs larger in size
gastric analysis

223
Q

treatment of megaloblastic anemia

A

vit B12 injections
oral/sublingual/nasal vit B12

224
Q

hemolytic anemia (def and causes)

A

excessive/premature destruction or hemolysis of RBC
increase of erythropoiesis

causes:
idiopathic
autoimmunity
infections
genetics
blood transfusion reactions

types:
sickle cell
thalassemia

225
Q

sickle cell anemia

A

genetic
crescent shaped
abnormal S hemoglobin
fragile, stiff, distorted
deliver les oxygen
clog and break into pieces
1 in 600 AA

226
Q

RBC lifespan in sickle cell

A

16 days

227
Q

sickle cell triggers

A

dehydration
stress
high altitude
fever
cold
physical excretion

228
Q

sickle cell manifestations

A

start at 4-5 months and live through 50’s
vessel occlusion
swelling in hands and feet with fever
sudden painful episodes

other complications dependent on area of occlusion

229
Q

treatment of sickle cell

A

no known cure

prevention:
avoid triggers
oxygen therapy
pain meds, relaxation
blood transfusions
bone marrow transplant
all recommended vaccinations
stem cell transplant
drugs: hydroxyurea - synthesis of more normal Hb

230
Q

thalassemia (def)

A

genetic
absence of alpha or beta globin
mediterranean descent
hypercoagulability - compensation - hyperplasia
hemolytic

231
Q

clinical features of thalassemia

A

delayed growth
osteoporosis
jaundice
dark urine
cardiomegaly
heart failure
hepatomegaly
splenomegaly
infections
poor appetite

232
Q

thrombocytosis

A

increased platelets

treatment:
platelet lowering drugs
aspirin

233
Q

thrombocytopenia

A

decreased platelets levels
increased risk of bleeding and infection

history of:
bruising
purpura
petechiae
bleeding from gums
nose bleeds
melena
abnormal menstrual bleeding

234
Q

what is hemophilia?

A

inherited bleeding disorder that results in decreased coagulation
X chromosome
1 in 500 males

235
Q

what are the symptoms of hemophilia?

A

bleeding in soft tissue, GI and joints
petechiae

236
Q

treatment of hemophilia

A

transfusion
bleeding precaution

237
Q

leukocytosis

A

increased WBCs

238
Q

leukocytopenia

A

decreased WBCs

239
Q

neutropenia

A

decreased number of circulating neutrophils

240
Q

neutrophilia

A

increase in number of circulating neutrophils

241
Q

lymphocytosis

A

increased lymphocytes

242
Q

lymphocytopenia

A

decreased lymphocytes

243
Q

leukemia

A

cancer of leukocytes

244
Q

what two systems are responsible for homeostasis?

A

nervous
endocrine

245
Q

what is phosphorylates protein?

A

for physiologic actions

246
Q

what is needed for a hormone reaction in a cell?

A

enzyme
protein
phosphate

each cell and hormone will need something different

247
Q

dose response relationship

A

magnitude of response correlates with hormone concentration

248
Q

down regulation

A

decreased affinity of receptors

249
Q

up regulation

A

increased affinity of receptors

250
Q

name the 8 endocrine glands

A

hypothalamus
adrenal
pituitary
thyroid
parathyroid
pancreas
pineal
thymus

251
Q

negative feedback

A

secretion inhibited when sensed to be high
called self limiting
short and long loops

252
Q

positive feedback

A

make more when not enough
VERY SPECIAL
breastfeeding and contractions

253
Q

anterior pituitary hormones

A

FSH
LH
TSH
ACTH
prolactin
GH

254
Q

posterior pit hormones

A

ADH
oxytocin (making it all okkk)

255
Q

hypothalamic pituitary relationship

A

links nervous and endocrine systems
infundibulum links the two

256
Q

post pit

A

neural tissue
collection of nerve axons
hormones stores in bulbous nerve terminals

257
Q

ant pit

A

collection of endocrine cells

258
Q

what are trophic hormones?

A

hormones that regulate secretion of other hormones

259
Q

somatotropin

A

ant
stim growth

260
Q

thyroid stimulating hormone

A

ant
stim synthesis and secretion of thyroid hormones
(T)

261
Q

follicle stimulating hormone

A

ant
secretes estrogen and maturation of sperm
(T)

262
Q

lutenizing hormone

A

ant
promotes ovulation, syn of estrogen, progesterone, and testosterone
(T)

263
Q

prolactin

A

ant
stim milk production and secretion

264
Q

adrenocorticotrophic hormone

A

ant
stim syn and secretion od adrenal cortical hormones
(T)

265
Q

antidiuretic hormone

A

post
makes kidneys reabsorb water

266
Q

oxytocin

A

post
stim contractions in uterus

267
Q

hormones released by hypothalamus: name action

thyrotropin-releasing hormone (TRH)
corticotropin-releasing hormone
gonadotropin-releasing hormone
somatotropin-release inhibiting hormone
growth hormone-releasing hormone
dopamine or prolactin-inhibiting hormone

A

stim pro of TSH and prolactin
stim pro of ACTH
stim sec of LH and FSH
inhib sec of GH
stim sec of GH
inhib sec of prolactin

268
Q

how to assess hypothalamic pituitary function

A

serum cortisol
serum prolactin
serum TSH
serum sex hormones
serum GH
MRI

269
Q

hypofunction of endocrine function

A

absence / impaired development of gland
impaired hormone synthesis
destruction of gland
hormone resistance

270
Q

hyperfunction of endocrine function

A

excessive stimulation because of hyperplasia or tumor

271
Q

three levels of altered endocrine function

A

primary: dysfunction of target gland
secondary: gland not receiving appropriate stim
tertiary: defect in hypothalamus

272
Q

hypopituitarism

A

decreased secretion of pit hormones

pit surgery/radiation
infections
infarction
hemorrhage
genetic disease

273
Q

anterior pituitary hypofunction

A

go look for the adenoma (order in loss)

GH
LH
FSH
TSH
ACTH

needs hormone replacement therapy

274
Q

facts about growth hormone

A

aka somatotropin
most important for normal growth
stim by GHRH
sec not constant over lifetime - more at puberty

275
Q

actions of GH

A

growth of all tissue
increases rate of protein synthesis
increased in fatty acid metabolism
decreased use of glucose as fuel

276
Q

what are IGFs?

A

insulin growth factors

keeps balance of the growth hormones

277
Q

what is IGF-1?

A

created when liver digests GH
has in indirect effect on growth

278
Q

GH deficiency in children

A

height less then 3rd % is pituitary dwarfism

279
Q

GH excess in children

A

gigantism
excess GH before puberty
excessive skeletal growth
meds: decrease GH level

280
Q

GH excess in adults

A

acromegaly
excess after long bone fushion
very rare

common casue:
adenoma of pit gland
hypothalamic tumors that sec GHRH

281
Q

clinical manifestations of acromegaly

A

bones cannot grow taller so get thicker
enlargement of small bones
bulbous nose
protruding lower jaw
teeth splayed
deepening of voice
degen arthritis
enlargement of heart
sleep apnea
menstrual irregularities
paresthesia’s
alteration in fat and carb metabolism
bitemporal hemianopia

282
Q

diagnosis of acromegly

A

clinical manifestations
serum GH/IGH-1
MRI/CT to localize lesion

283
Q

treatment of acromegaly

A

normalization of GH/IGF-1 levels
removal of tumor
dopamine agonist drugs
GH receptor blocker

284
Q

antidiruetic hormone facts

A

aka vasopressin
regulates body fluid osmolarity
increases water reabsorption
stimulated by decrease in ECF volume

285
Q

diabetes insipidus

A

condition of ADH
inability of the body to concentration or retain water

286
Q

causes of DI

A

injury to hypothal
injury to neurohypophyseal tract
injury to post pit gland
inadequate kidney response to presence of ADH
excessive consumption of fluids
damage of thirst regulating mech

287
Q

clinical presentations of DI

A

polyuria
nocturia
polydipsia (increased thirst)
dehydration

288
Q

diag of DI

A

history
recent injury to brain
ADH levels
urine osmolality

289
Q

treatment of DI

A

hydration
antidiuretic meds

290
Q

DI and PT

A

often fatigue, have muscle pain and weakness
less willing to do therapy
find something they like and want to do
hydrate regularly and have restroom accessible
education to prevent edema

291
Q

red flags in DI

A

paleness
dizziness
lightheadedness
extreme hypotension
fever

292
Q

syndrome of inappropriate ADH

A

excessive release of ADH
water intoxication
hyponatremia

293
Q

diag of SIADH

A

hyponatremia
plasma osmolality
decreased urine output
concentrated urine

294
Q

treatment of SIADH

A

removal of cause
meds to increase urine output (hughes’ piddle pill)
monitor for weight gain
fluid restrictions
hypertonic IV solution

295
Q

PT and SIADH

A

cautious of water intake
cautious of intensity/physical exertion
watch for water intoxication

296
Q

DI, if left untreated will rapidly develop into:

A

dehydration

297
Q

describe the adrenal glands

A

located above kidneys
aka suprarenal
two layers: cortex and medulla

298
Q

what hormones does the adreanl medulla secrete?

A

catecholamines
epi and norepi

299
Q

what hormones does the adrenal cortex secrete?

A

adrenocorticoids

300
Q

what hormones does the zona glomerulosa secrete?

A

mineralocorticoids

301
Q

what hormones do the zonas reticularis and fasciculata secrete?

A

glucocorticoids and androgens

302
Q

what do mineralocorticoids do?

A

regulate reabsorbance of Na
secretion of K by kidneys
water balance
blood pressure

303
Q

what do glucocorticoids do?

A

regulate body’s response to stress
regulate protein, lipid and carbo metabolism
regulate blood glucose levels and immune response

304
Q

what do adrenal androgens do?

A

regulate reproductive function
regulate pubic and axillary hair growth

305
Q

describe the structure of adrenocorticoids?

A

basic structure of cholesterol
carbons 1-21
4 rings

306
Q

biosynthesis pathway of adrenal cortex

A

cholesterol desmolase stimmed by ACTH

cortisol is not necessary for life if corticosterone is being synthesized

307
Q

regulation of secretion of adrenocortical steriods

A

regulated by hypothalamic-piuitary axis
negative feedback
glom depends ACTH for first step but otherwise controlled by renin-angiostensin-aldosterone system

308
Q

describe the diurnal secretion pattern of cortisol

A

lowest secretion just after falling asleep
higher secretion just before awakening

309
Q

actions of aldosterone

A

incres sodium reabsorption
incres potassium excretion
incres hydrogen excretion

310
Q

what happens when there is an increased in aldosterone levels?

A

ECF volume expansion and hypertension
hypokalemia
metabolic alkalosis

311
Q

describe the two systems that regulate aldosterone secretion.

A

renin-angiotensin II-aldosterone:
angio II increases synthesis and secretion of aldosterone by stimming cholestorol desmolase and aldosterone synthase

serum K concentration:
increase serum K increases aldosterone secretion

312
Q

function of glucocorticoids

A

essential for life!!
contribute to stress response
decreases tissue glucose utilization
incres breakdown of proteins
incres mobilization of fats
inhibit edema formation
inhibit immune and inflam effects
inhibit bone formation
stim gastric secretion

313
Q

actions of adrenal androgens for each gender

A

males:
minor role
synthesis of testosterone in testes is much greater

female:
major role
no hormone production in female sex organs

314
Q

how do you test adrenal function?

A

blood levels of ACTH, cortisol, aldosterone, CRH
urine specimen to test excretion

315
Q

adrenal cortical insufficiency (pri, sec, ter)

A

primary:
destruction of adrenal gland

secondary:
lack ACTH - disorder of pit gland

tertiary:
lack of CRH - hypothal defect

316
Q

what happens in acute adrenal crisis?

A

caused by:
trauma, hemorrhage, thrombosis

serious, life threatening, severe hypotension, shock, death

317
Q

what is addison’s disease and what causes it?

A

primary adrenal insuff
adrenal cortical hormones are deficient and ACTH levels are elevated

causes:
autoimmune destruction
TB
fungal infection
adrenal hem from anticoags

318
Q

clinical manifestations of Addison’s disease categorized by hormone

A

min:
hyponatremia
loss of ECF
decres cardiac output
hyperkalemia
orthostatic hypotension

glu:
porr tolerance to stress
hypoglycemia
GI symptoms

And:
women have sparse axillary and pubic hair

319
Q

when are symptoms apparent in addison’s

A

when 90% of gland has been destroyed

320
Q

clinical manifestations of addisons that are not hormone specific

A

increased ACTH
increased pigmentation over backs of hands, lips and mouth

in whites:
slight tan, black freckles, intense general pigmentation

in blacks:
slate-gray color

321
Q

what is an adrenal crisis and what are the symptoms?

A

extreme stress without steroid coverage
need to be injected with glucocorticoids

symptoms:
severe drop in BP causing dizziness
light headedness
GI stuff
confusion and lethargy
muscle cramps and weakness

322
Q

diagnosis of addisons

A

sodium, potassium, corticosteroid levels

323
Q

treatment of addisons

A

replacing fluids, electrolytes, glucose and cortisol
IV fluid replacement
lifetime therapy - oral or hydrocortisone
DHEA in females

324
Q

exercise interventions with addisons

A

fatigue easily
30 min aerobic routine with strengthening
modulate symptoms
pt to listen to body
educate

325
Q

what is cushing syndrome and what causes it?

A

excess glucocorticoid production

causes:
adrenal gland tumor
ectopic production
glucocorticoid drugs

326
Q

when does cushing syndrome become cushing’s disease?

A

tumor of pituitary gland - excess production of ACTH

327
Q

clinical manifestations of cushing

A

protein breakdown: muscle wasting, protuberant abdomen
moon shaped face
thinning of skin with purple striae on breast
altered calcium metabolism
poor wound healing
decreased immune response
persistent hyperglycemia - steroid diabetes
increases gastric acid secretion
increase mineralocorticoid
increase androgens
memory/concentration/cognition

328
Q

diagnosis of cushing

A

24 hour urinary cortisol
late night salivary cortisol
imaging of pit and adr glands

329
Q

treatment of cushing

A

correct the source
after removal, cortisol replacement therapy to help it catch up
drugs that block synthesis if there is a tumor
precautions to minimize infection

330
Q

exercise interventions with cushing

A

management of osteoporosis
balance training
resistance training
improving ROM
sling therapy
aerobic exericse

Spring A 2025 (6 decks)

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