patho exam 1 Flashcards
urinary system
two kidneys
two ureters
urinary bladder
urethra
where do the kidneys lie?
on the rear wall of abdomen
T12-L3 level
how much cardiac output do the kidneys receive?
20%
what are the primary functions of the kidneys?
filter blood and produce urine
regulation of plasma ionic composition
regulation of plasma volume
regulation of plasma osmolarity
regulation of plasma hydrogen ion concentration
what are the secondary functions of the kidney?
secrete erythropoietin
secrete renin
activate vitamin D3
what does a nephron consist of?
renal corpuscles
renal tubule
superficial/cortical nephron
entirely within cortex
juxtamedullary nephron
15-20% of all
what is the first step in formation of urine?
glomerular filtration
names for the fluid that is filtered
filtrate
glomerular filtrate
ultrafiltrate
what does filtrate consist of?
water and small solutes
does not have:
blood cells and proteins
what are the starling forces
two hydrostatic and two oncotic pressures
what forces favor filtration?
glomerular HP
bowman’s OP
what forces oppose filtration?
bowman’s HP
glomerular OP
what is oncotic pressure?
pressure due to the presence of proteins in the blood
what GFR is considered kidney failure?
less than 15%
filtration
bulk flow of protein free plasma from glom capillaries into bowman’s capsule
reabsorption
water and solutes reabsorbed from glomular filtrate into peritubular capillary
secretion
net result of processes of filtration, reabsorption and secretion
normal values for routine urinalysis
color - yellow amber
appearance - clear to slightly hazy
volume - 600-2500ml/24 hrs
glucose - neg
ketones - neg
protein - neg
RBC - neg
WBC - neg
GFR (glomular filtration rate)
very timed manner of collecting blood and urine
now using estimated GFR
serum creatinine
waste product of muscle metabolism
if SC doubles, GFR has fallen to 1/2
blood urea nitrogen
end product of protein metabolism
indicator of liver and kidney function
2/3rd renal function lost before sig rise
possible etiologies with proteinuria
renal failure
nephrotic syndrome preeclampsia
renal artery/vein thrombosis
glomerular disease
tubulopathy
possible etiologies with glucosuria
diabetes mellitus
possible etiologies with ketonuria
diabetes mellitus
ketoacidosis
starvation
possible etiologies with hematuria
glomerular damage
tumors
kidney trauma
urinary tract infection
acute tubular necrosis
urinary tract obstruction
possible etiologies with pyuria
upper and lower urinary tract infection
acute golmerulonephritis
renal calculi
possible etiologies with bacteruria
upper and lower urinary tract infection
polycystic kidney disease
fluid filled sacs
single or multiple
progressive
inherited or acquired
autosomal dominant polycystic kidney disease
account for 10% of ESRD, 4th leading cause
thousands of fluid sacs
slow progression
kidneys enlarged and misshapen
most common PKD
manifestations of ADPKD
pain
infected cysts
hematuria
enlarged kidneys
hypertension
headaches, nauseam vomiting
hemorrhages
autosomal recessive polycystic kidney disease
1 in 20,000 live births
mutation in PKHD1
evident at birth
restricts lung development
10 year survival rate beyond 1 year of life
glomerulonephritis
affects men more than women
leading cause of chronic kidney disease
nephritic vs nephrotic
nephrotic syndrome
inflammation occludes glom capillary lumen
clinical findings of nephrotic syndrome
massive proteinuria
hypoalbuminemia
generalized edema
dyspnea
hyperlipidemia
lipiduria
dark, cloudy urine
nephritic syndrome
circulating immune complexes become trapped in glomerular membrane
clinical manifestations of nephritic syndrome
hematuria
proteinuria
low GFR
azotemia
oliguria
hypertension
treatment of glomerulonephritis
antibiotics
corticosteroids
blood pressure management
temporary dialysis
chronic kidney disease
1 in 9 adults
gradual irreversible loss of renal function
3+ months
unable to regulate fluid and electrolytes
GFR less than 60ml/min
most common causes of CKD
diabetes mellitus
hypertension
glomerulonephritis
PKD
stage 1 kidney failure
no overt symptoms
unaffected nephrons hypertrophy
hypertension and anemia
stage 2 kidney failure
small amount of albumin is excreted in urine
stage 3 kidney disease
albumin levels increase in urine and decrease in blood
increase of waste in blood - azotemia
stage 4 and 5 kidney failure
complications appear
proteinuria
hypertensive
stage 5 kidney failure
cannot excrete toxins
uremia
all systems affected
red flags of CKD
recurrent infections
edema
numbness
trouble breathing
ulcerations
heart failure
platelet dysfunction
hypertension
memory loss
seizures
renal osteodystrophy
clinical manifestations of kidney failure
tired, weak, pale skin
itchy, dry skin, less sweating
metallic taste
hypertension
platelet dysfunction
anorexia, nausea
electrolyte imbalances
respiratory distress
infections
memory loss
osteodystrophy
diagnosis of CKD
initial symptoms are vague
tests: CBC, BUN, CT, MRI
treatment of kidney failure
prevention: control diabetes, hypertension
treat underlying disease
protein restriction
adequate fat and carbs
potassium restriction
remain hydrated
dialysis
transplant
hemodialysis
in clinic
cleanses the blood
peritoneal dialysis
can be done at home
ambulatory: 4 times a day
cycle assisted: machine, during sleep, 7-10 hrs
precautions when on dialysis
keep dialysis site clean and dry
staying properly hydrated
avoid overexertion
staying aware of cognitive and physical state
preferred when dialysis not running
red flags when on dialysis
acute infection or fever
hypotension
chest pain or SOA
bleeding at dialysis site
abnormal hearth rhythms
decreased consciousness
kidney transplant
primary indication is T1D with ESRD
younger than 45
less expensive than LT dialysis
5 year survival rate for pancreas-kidney transplant
95%
5 year survival rate for kidney transplant
88%
PT and CKD
high risk of CVD
PT helps manage symptoms and manifestations
suggest to burn 1000 Kcal a week
barriers/contraindications to PT with CKD
previous experiences with exercise
time
sick role - may exacerbate, accepting fate
pain/fatigue/lethargy
motivation
post op recovery
uncontrolled CVD, DM
infection
recommendations for PT with CKD
30 min 3-5x/week
muscle strengthening, flexibility, balance
increase difficulty
cardiovascular - biking
dialysis is best when combines with what?
aerobic and resistance exercise
what to look out for when working with dialysis pts?
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
define pathophysiology
study of functional changes that occur in the body as a result of the mechanism of disease
define pathogenesis
development of cellular events and reactions,
development of the disease
what does the cell membrane do?
protection
selective permeable - decides what goes in and out
function of nucleus
control center
function of nucleolus
produces RNA
function of endoplasmic reticulum
synthesizes enzymes and proteins
function of ribosomes
aid in protein protection
function of golgi proteins
sorts, modifies, and packages proteins
function of lysosomes
digests waste
function of mitochondria
produces ATP
where is epithelial tissue found?
outer surface of body
lines GI
lines respiratory
lines blood vessels
functions of epithelial tissues
barrier, protection
absorption
filtration
secretion
permeability
regeneration
3 types of epithelial tissues
squamous: thin and flat
cuboidal: cube shape
columnar
location of cuboidal cells
surface of ovary and thyroid
location of columnar cells
lines intestines
3 ways to describe layers of epithelial cells
simple: one layer
stratified: multiple layers
pseudostratified: looks like multiple but actually one
location of three types of simple epithelial cells
Sim squam: lines blood vessels, lymph nodes, alveoli
Sim cub: glands
Sim col: digestive tract
location of three types of stratified epithelial cells
Strat squam: skin
Strat cub: sweat and salivary glands
Strat col: (VERY RARE) conjunctiva
pseudostratified epithelial tissue
all cells in contact with underlying matrix
not all extend to surface
P col: most of upper respiratory tract
transitional epithelium
can change shape when stretched
ex: urinary bladder, urethra, ureters
components of connective tissue
cells
extracellular protein fibers
ground substance
examples of connective tissue
tendons
ligaments
adipose tissue
cartilage
bone
blood and lymph
marfan syndrome
CT disorder
1 in 5,000 people
damages blood vessels, hearts, eyes skin, lungs, and bones
tall slender build
flat feet
aortic aneurysm common
describe skeletal muscle
long and cylindrical
striated
voluntary
describe smooth muscle
visceral organs
nonstriated
spindle shape
invol
intercalated disks/gap junctions
describe cardiac muscle
shorter, branched
invol
striated
intercalated disks/gap junctions
skeletal muscle layers (inside to out)
endomysium
perimysium
epimysium
describe the three troponins
T - attaches troponin to tropomyosin
I - inhibits interaction between actin and myosin
C - calcium binding protein
function of transverse tubules
action potential travels through
function of sarcoplasmic reticulum
around myofibrils
accumulates calcium
keeps intercellular calcium concentration low when at rest
steps in excitation contraction coupling
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
steps in cross bridge cycle
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
length-tension relationship
need just enough overlap but not 100% shortened or lengthened
facts about cardiac muscle
muscle cells - cardiomyocytes
increase in troponin is used to diagnose heart attack
facts about smooth muscle
invol
lacks striations
found in walls of hollow organs
produces motility
maintains tension
calcium binding protein called calmodulin
which portion of sarcomere’s length remains same during excitation contraction coupling?
A band
which is not related?
skeletal
striated
visceral
voluntary
visceral
which is not related?
smooth
visceral
voluntary
organs
voluntary
which is not related?
cardiac
branching
visceral
involuntary
visceral
define reversible cell injury
cell is able to recover homeostasis after removal of stress
atrophy
decreased cell size
causes: disuse, denervation
cerebral atrophy
reduction of size of brain cells in cerebrum
causes: TBI, infections
hypertrophy
increased cell size
seen in cardiac and skeletal muscle
causes: increase workload, increased hormones
hyperplasia
increased cell number
seen in epidermis, intestinal epithelium
cause: hormonal signaling and increase in work load
metaplasia
conversion of one cell type to another
cause: irritation, inflammation
cigarette smoker
GERD
dysplasia
disorderly growth
precursor of cancer
what if the cells do not have the ability to adapt to stressors?
cell death
irreversible cell injury
alterations in cell nucleus
rupture of cell membrane
release of digestive enzymes
release contents to ECF
reversible cell injury
swelling
membrane blebs
define necrosis
damaged cells
initiates inflammation
define apoptosis
programmed cell death
does not initiate inflammation
3 lines of defense for immunity
skin and mucous membrane
inflammation
immunity
function of neutrophil
inflammation
defense against foreign substances like bacteria, fungi
function of monocytes
immature macrophages
clean up debris/damaged cells
eosinophils
attack parasites, cancer cells
play a role in asthma and allergy
basophils
produce allergic response like sneezing
lymphocytes (T and B)
immunity
produce antibodies
kills antigens
purpose of inflammation
essential to healing
paves to way for repair of injured tissue
acute inflammation
expected response to injury
restoration of tissue homeostasis
vascular and cellular phase
chronic inflammation
days to years
unrelenting injury
cells involved: monocytes, macrophages, fibroblasts
only have symptoms during flare ups
cardinal signs of inflammation
rubor (redness)
tumor (swelling)
calor (heat)
dolor (pain)
functio lasea (loss of function)
systematic manifestations: fever, leukocytosis
vascular phase
marked by tissue edema
constriction followed by dilation
increased permeability
swelling, pain, impaired function
cellular phase
chemotaxis
adhesion to endothelium
transmigration across endothelium
what cells are active in cellular phase?
WBC
RBC
platelets
CT cells
ECM - elastin, collagen
what mediators cause vasodilation
prostaglandins
histamine
nitric oxide
what mediators cause vascular permeability
histamine
bradykinin
leukotrienes
PAF
what mediators cause pain
prostaglandins
bradykinins
what mediators cause fever
prostaglandins
what mediators cause leukocytosis
leukocytes
mast cells and eosinophils
granulocytes
monocytes
natural killer cells
what mediators limit inflammation
histaminase
kinases
what mediators repair and heal
TGF -B
angiogenic factors
what mediators cause phagocytosis
leukotrienes
how does WBC change with inflammation?
increase
how does c-reactive protein change with inflammation?
increase
how does prothrombin (time to coagulate) change with inflammation?
reduced
coag faster
how does fibrinogen change with inflammation?
increased
needed for fibrin to cause clotting
how does WBC differential change with inflammation?
neutrophils increase in acute inflammation
how does ESR change with inflammation?
increase often above 100mm/hr
erythrocyte sedimentation rate - how fast blood samples sediments in a tube in an hour
nonspecific
CRP
synthesized in liver
nonspecific, but more accurate than ESR
sequence of cell injury
irritant enters
cell damage
inflammatory mediators
blood vessels dilate
redness, heat, edema
WBC migrate
phagocytosis
two ways of tissue repair
regeneration: injured cells replaces with healthy
replacement with CT (scar)
phases of wound healing
inflammation - 5-10 days
proliferation and migration - 3-20 days
remodeling and maturation - past 21 days
components of tissue healing
fibronectin - helps with blood clot
proteoglycans - hydration
elastin
collagen - support and tensile strength
factors that affect tissue healing
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
arginine
enhances healing and immune function
migration of phagocytic white blood cells into injured area: what comes next?
neutrophils come first to remove bacteria
macrophages in 24 hrs
release growth factors for proliferative stage
form granulation tissue
angiogenesis
formation of new blood vessels
granulation tissue
reddish granular layer of tissue
re-epithelialization
proliferate to form new surface layer
filling in gap in the wound
makes a scab
remodeling phase
3 weeks after injury
red to pink to white
factors that impact wound healing
inflammatory/immune response
inadequate nutritional status
poor tissue perfusion
complications of wound healing and tissue repair
infection
ulceration
adhesions
dehiscence (wounds pull apart)
keloid development
wound healing continuum colors
black- dead
yellow- infection
red- healing in granulation phase
pink- healing, re-epi
what is a granuloma?
form chronic inflammation
when injury is too difficult to control
lymphocytes attempt to surround foreign body
difference between time in acute and chronic inflammation
acute: resolution within a few weeks
chronic: present for prolonged period of time
difference between chief phagocytic cells in acute and chronic inflammation
acute: neutrophils
chronic: monocytes, macrophages
difference between restoration in acute and chronic inflammation
acute: minimal scarring
chronic: marked by fibrosis, scarring or granulation
you get a papercut and experience pain at the site. this response is related to:
increases exudate and chemical mediators at the site
antigens
any foreign substance that elicits an immune response
antibody
responds to antigens
innate immunity
born with it
1st reponder
rapid and always the same
nonspecific
non adaptive
acquired/adaptive immunity
slower response
diverse
specific
has memory
self and non self recognition
active acquired immunity
get sick
vaccine
passive acquired immunity
transferred from person to person
ex: mother to fetus
two types of cells in adaptive/acquired immunity
humoral - B
cell mediated - T
how to B and T cells move through the body?
migrate through blood, lymph and lymph nodes
humoral immunity
involves antibodies/immunoglobulins
B cells originate and mature in bone marrow
cell mediated immunity
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
factors altering the immune system
aging
nutrition - vit A and E, zinc
burns - decrease neutrophil function
sleep disturbances
illness and disease
drugs
surgery/anesthesia
exercise immunology
mod intensity enhances immune function
neut, NK, lymphocytes all increase
immune system disorders
primary: defect involving cells
secondary: results from an underlying disease/factor
AIDS
first recognized in 1981, HIV in 1986
infects CD4, dendritic, macrophages
progressive destruction of T cells
immunodeficiency
pathophysiology of AIDS
transmitted through bodily fluids
risk factors include: poverty, drugs, bad health care
pathogenesis of AIDS
retrovirus
attacks and inactivates CD4
high mutation rate
continual destruction of CD4
progressive loss immune function
steps to pathogenesis of AIDS
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
HIV spectrum
asymptomatic: CD4 count >500
symptomatic: CD4 count 200-500
advanced: <200
normal is 600-1200
clinical manifestation of HIV
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
dermatologic conditions of AIDS
hair loss
rash
delayed wound healing
dry flaking skin
kaposi sarcoma - purple cancer
diagnosis of HIV/AIDS
screening in individuals aged 13-64 yrs
blood tests or oral fluid
treatment for HIV/AIDS
no cure
HAART - highly active antiretroviral therapy
NSAIDS and pain meds
possible vaccines in the future
entry inhibitors
block HIV from connecting to CD4
nukes and non nukes
stop HIV changing from RNA to DNA
integrase inhibitors
block HIV from being integrates into cell’s DNA
protease inhibitors
block new HIV from being cut into smaller proteins
special implications for the therapist (HIV/AIDS)
women victim of domestic violence
msk or neuro problems with unknown origin
exercise and HIV
moderate is good
strenuous is bad
management of physical dysfunctions
regular exercise encouraged
address impairment
monitor response to exercise
avoid overtraining
post exposure prophylaxis
call CDC
28 days course of HAART
avoid spreading your fluids
hypersensitivity type 1
IgE mediated
most common
immediate
severe - anaphylactic shock
hypersensitivity type 2
IgG, IgM mediated
antibody mediated
basis of autoimmune disease
hypersensitivity type 3
IgG, IgM, complement mediated
formation of antigen-antibody immune complexes
massive inflammatory response
hypersensitivity type 4
T cell mediated
delayed
transplant rejection
autoimmune disorders (hypersensitivity type 2)
addison’s
crohn’s
T1D
polymyositis/dermatomyositis
thyroiditis
ulcerative colitis
MS
MG
RA
systemic lupus erythematosus
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
facts about blood
is CT
has cells suspended in liquid matrix
5 liters in the body
7-8% of total body weight
blood composition: overview
plasma - 55%
red blood cells
platelets
white blood cells
components of plasma
proteins - 7%
water - 91.5%
other solutes - 2%
what proteins are in blood?
albumin - 54%
fibrinogen - 7%
globulins - 38%
others - 1%
what “other solutes” are present in blood?
electrolytes
hormones, enzymes
nutrients, carbohydrates, fats
gases
waste products
what is the function of plasma?
transport nutrients, chemical messengers and metabolites
what is the function of albumin?
maintains plasma oncotic pressure
maintains blood volume
serves as a carrier
what is the function of globulins?
alpha - transports bilirubin
beta - transports iron
gamma - anitbodies of immune system
what is the function of fibrinogen?
helps form fibrin for clotting
plasma vs serum
plasma - treated with anti-coagulants
serum - liquid after coagulation
facts about red blood cells
most common blood cells
transport oxygen to tissues and co2 out of tissues
each hemoglobin carries for oxygens
productions in bone marrow
what is the life span of RBCs
about 120 days
iron is recycles in small intestine after cell death
globin is recycled
heme turns to bilirubin and is excreted
hematocrit
percent of RBCs in blood
women: 37-47
men: 42-52
anemia - not enough
polycythemia - excess
anemia
common
abnormally low RBCs
causes of anemia
blood loss
destruction
inadequate or defective RBC production
reduction in hemoglobin content
abnormal hemoglobin
general features of anemia
weakness
fatigue
dyspnea
hypoxia of brain tissue
pallor - absence of red
tachycardia
severe - heart failure
increased respiration rate
bone pain
3 types of anemia
iron deficiency
megaloblastic
sickle cell disease
iron deficiency anemia (definition and causes)
iron does not meet demands of hemoglobin production
causes:
decreased iron consumption
increased iron demand
where is iron stored?
ferritin
transferrin
what groups are at risk for iron deficiency anemia?
pregnant women
women with heavy menstrual bleeding
infants and younger children
frequent blood donors
cancer, GI, surgical pts
vegetarian diet
features of iron deficiency anemia
fatigue
brittle nails
headache
delayed healing
tachycardia
decreased appetite
unusual food cravings
neuro impairment or damage
IDA diagnosis
low hemoglobin and hematocrit
RBCs microcytic and hypochromic
serum ferritin
serum iron
IDA treatment
treating cause
consuming iron rich foods
iron supplements
high vitamin c for absorption
megaloblastic anemia (definition and causes)
impaired DNA synthesis - large immature RBCs
causes:
B12 deficiency - decreased cell division & maturation
folic acid deficiency
megaloblastic - pernicious anemia
absence of intrinsic factors in stomach
inhibits absorption of B12
features of megaloblastic anemia
bleeding gums
diarrhea
anorexia
demyelination
paresthesia of hands and feet
impaired sense of smell
personality/memory changes
mild jaundice
diagnosis of megaloblastic anemia
serum vitamin B12
CBC
IF antibodies
RBCs larger in size
gastric analysis
treatment of megaloblastic anemia
vit B12 injections
oral/sublingual/nasal vit B12
hemolytic anemia (def and causes)
excessive/premature destruction or hemolysis of RBC
increase of erythropoiesis
causes:
idiopathic
autoimmunity
infections
genetics
blood transfusion reactions
types:
sickle cell
thalassemia
sickle cell anemia
genetic
crescent shaped
abnormal S hemoglobin
fragile, stiff, distorted
deliver les oxygen
clog and break into pieces
1 in 600 AA
RBC lifespan in sickle cell
16 days
sickle cell triggers
dehydration
stress
high altitude
fever
cold
physical excretion
sickle cell manifestations
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
treatment of sickle cell
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
thalassemia (def)
genetic
absence of alpha or beta globin
mediterranean descent
hypercoagulability - compensation - hyperplasia
hemolytic
clinical features of thalassemia
delayed growth
osteoporosis
jaundice
dark urine
cardiomegaly
heart failure
hepatomegaly
splenomegaly
infections
poor appetite
what is aplastic anemia?
body does not produce RBCs
rare but very serious
PT and anemia
start slow
aerobic exercise
5-10 min at a time
stretching - yoga or tai chi
light resistance if appropriate
thrombocytosis
increased platelets
treatment:
platelet lowering drugs
aspirin
thrombocytopenia
decreased platelets levels
increased risk of bleeding and infection
history of:
bruising
purpura
petechiae
bleeding from gums
nose bleeds
melena
abnormal menstrual bleeding
what is hemophilia?
inherited bleeding disorder that results in decreased coagulation
X chromosome
1 in 500 males
what are the symptoms of hemophilia?
bleeding in soft tissue, GI and joints
petechiae
treatment of hemophilia
transfusion
bleeding precaution
PT and hemophilia
aerobic
strength
ROM
fascial treatment
hydrotherapy
proprioception training
balance training
CO2 laser therapy
KT taping
PT education and hemophilia
steering away from contact sports
know signs and symptoms
yearly exam to check blood
leukocytosis
increased WBCs
leukocytopenia
decreased WBCs
neutropenia
decreased number of circulating neutrophils
neutrophilia
increase in number of circulating neutrophils
lymphocytosis
increased lymphocytes
lymphocytopenia
decreased lymphocytes
leukemia
cancer of leukocytes
what two systems are responsible for homeostasis?
nervous
endocrine
what is phosphorylates protein?
for physiologic actions
what is needed for a hormone reaction in a cell?
enzyme
protein
phosphate
each cell and hormone will need something different
dose response relationship
magnitude of response correlates with hormone concentration
down regulation
decreased affinity of receptors
up regulation
increased affinity of receptors
name the 8 endocrine glands
hypothalamus
adrenal
pituitary
thyroid
parathyroid
pancreas
pineal
thymus
negative feedback
secretion inhibited when sensed to be high
called self limiting
short and long loops
positive feedback
make more when not enough
VERY SPECIAL
breastfeeding and contractions
anterior pituitary hormones
FSH
LH
TSH
ACTH
prolactin
GH
posterior pit hormones
ADH
oxytocin (making it all okkk)
hypothalamic pituitary relationship
links nervous and endocrine systems
infundibulum links the two
post pit
neural tissue
collection of nerve axons
hormones stores in bulbous nerve terminals
ant pit
collection of endocrine cells
what are trophic hormones?
hormones that regulate secretion of other hormones
somatotropin
ant
stim growth
thyroid stimulating hormone
ant
stim synthesis and secretion of thyroid hormones
(T)
follicle stimulating hormone
ant
secretes estrogen and maturation of sperm
(T)
lutenizing hormone
ant
promotes ovulation, syn of estrogen, progesterone, and testosterone
(T)
prolactin
ant
stim milk production and secretion
adrenocorticotrophic hormone
ant
stim syn and secretion od adrenal cortical hormones
(T)
antidiuretic hormone
post
makes kidneys reabsorb water
oxytocin
post
stim contractions in uterus
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
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
how to assess hypothalamic pituitary function
serum cortisol
serum prolactin
serum TSH
serum sex hormones
serum GH
MRI
hypofunction of endocrine function
absence / impaired development of gland
impaired hormone synthesis
destruction of gland
hormone resistance
hyperfunction of endocrine function
excessive stimulation because of hyperplasia or tumor
three levels of altered endocrine function
primary: dysfunction of target gland
secondary: gland not receiving appropriate stim
tertiary: defect in hypothalamus
hypopituitarism
decreased secretion of pit hormones
pit surgery/radiation
infections
infarction
hemorrhage
genetic disease
anterior pituitary hypofunction
go look for the adenoma (order in loss)
GH
LH
FSH
TSH
ACTH
needs hormone replacement therapy
facts about growth hormone
aka somatotropin
most important for normal growth
stim by GHRH
sec not constant over lifetime - more at puberty
actions of GH
growth of all tissue
increases rate of protein synthesis
increased in fatty acid metabolism
decreased use of glucose as fuel
what are IGFs?
insulin growth factors
keeps balance of the growth hormones
what is IGF-1?
created when liver digests GH
has in indirect effect on growth
GH deficiency in children
height less then 3rd % is pituitary dwarfism
GH excess in children
gigantism
excess GH before puberty
excessive skeletal growth
meds: decrease GH level
GH excess in adults
acromegaly
excess after long bone fushion
very rare
common casue:
adenoma of pit gland
hypothalamic tumors that sec GHRH
clinical manifestations of acromegaly
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
diagnosis of acromegly
clinical manifestations
serum GH/IGH-1
MRI/CT to localize lesion
treatment of acromegaly
normalization of GH/IGF-1 levels
removal of tumor
dopamine agonist drugs
GH receptor blocker
antidiruetic hormone facts
aka vasopressin
regulates body fluid osmolarity
increases water reabsorption
stimulated by decrease in ECF volume
diabetes insipidus
condition of ADH
inability of the body to concentration or retain water
causes of DI
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
clinical presentations of DI
polyuria
nocturia
polydipsia (increased thirst)
dehydration
diag of DI
history
recent injury to brain
ADH levels
urine osmolality
treatment of DI
hydration
antidiuretic meds
DI and PT
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
red flags in DI
paleness
dizziness
lightheadedness
extreme hypotension
fever
syndrome of inappropriate ADH
excessive release of ADH
water intoxication
hyponatremia
diag of SIADH
hyponatremia
plasma osmolality
decreased urine output
concentrated urine
treatment of SIADH
removal of cause
meds to increase urine output (hughes’ piddle pill)
monitor for weight gain
fluid restrictions
hypertonic IV solution
PT and SIADH
cautious of water intake
cautious of intensity/physical exertion
watch for water intoxication
DI, if left untreated will rapidly develop into:
dehydration
describe the adrenal glands
located above kidneys
aka suprarenal
two layers: cortex and medulla
what hormones does the adreanl medulla secrete?
catecholamines
epi and norepi
what hormones does the adrenal cortex secrete?
adrenocorticoids
what hormones does the zona glomerulosa secrete?
mineralocorticoids
what hormones do the zonas reticularis and fasciculata secrete?
glucocorticoids and androgens
what do mineralocorticoids do?
regulate reabsorbance of Na
secretion of K by kidneys
water balance
blood pressure
what do glucocorticoids do?
regulate body’s response to stress
regulate protein, lipid and carbo metabolism
regulate blood glucose levels and immune response
what do adrenal androgens do?
regulate reproductive function
regulate pubic and axillary hair growth
describe the structure of adrenocorticoids?
basic structure of cholesterol
carbons 1-21
4 rings
biosynthesis pathway of adrenal cortex
cholesterol desmolase stimmed by ACTH
cortisol is not necessary for life if corticosterone is being synthesized
regulation of secretion of adrenocortical steriods
regulated by hypothalamic-piuitary axis
negative feedback
glom depends ACTH for first step but otherwise controlled by renin-angiostensin-aldosterone system
describe the diurnal secretion pattern of cortisol
lowest secretion just after falling asleep
higher secretion just before awakening
actions of aldosterone
incres sodium reabsorption
incres potassium excretion
incres hydrogen excretion
what happens when there is an increased in aldosterone levels?
ECF volume expansion and hypertension
hypokalemia
metabolic alkalosis
describe the two systems that regulate aldosterone secretion.
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
function of glucocorticoids
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
actions of adrenal androgens for each gender
males:
minor role
synthesis of testosterone in testes is much greater
female:
major role
no hormone production in female sex organs
how do you test adrenal function?
blood levels of ACTH, cortisol, aldosterone, CRH
urine specimen to test excretion
adrenal cortical insufficiency (pri, sec, ter)
primary:
destruction of adrenal gland
secondary:
lack ACTH - disorder of pit gland
tertiary:
lack of CRH - hypothal defect
what happens in acute adrenal crisis?
caused by:
trauma, hemorrhage, thrombosis
serious, life threatening, severe hypotension, shock, death
what is addison’s disease and what causes it?
primary adrenal insuff
adrenal cortical hormones are deficient and ACTH levels are elevated
causes:
autoimmune destruction
TB
fungal infection
adrenal hem from anticoags
clinical manifestations of Addison’s disease categorized by hormone
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
when are symptoms apparent in addison’s
when 90% of gland has been destroyed
clinical manifestations of addisons that are not hormone specific
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
what is an adrenal crisis and what are the symptoms?
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
diagnosis of addisons
sodium, potassium, corticosteroid levels
treatment of addisons
replacing fluids, electrolytes, glucose and cortisol
IV fluid replacement
lifetime therapy - oral or hydrocortisone
DHEA in females
exercise interventions with addisons
fatigue easily
30 min aerobic routine with strengthening
modulate symptoms
pt to listen to body
educate
what is cushing syndrome and what causes it?
excess glucocorticoid production
causes:
adrenal gland tumor
ectopic production
glucocorticoid drugs
when does cushing syndrome become cushing’s disease?
tumor of pituitary gland - excess production of ACTH
clinical manifestations of cushing
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
diagnosis of cushing
24 hour urinary cortisol
late night salivary cortisol
imaging of pit and adr glands
treatment of cushing
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
exercise interventions with cushing
management of osteoporosis
balance training
resistance training
improving ROM
sling therapy
aerobic exericse
