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cushings cause

excess corticosteroid (any of the three)

cushings syndrome

excess prolonged administration of corticosteroids (giving pt the meds)

cushings disease

caused by ACTH secreting tumors of pituitary gland OR direct tumor of adrenal gland

ACTH

adrenocoticotropic hormone, made in pituitary, stimulates adrenal cortex to produce its hormones

cushings S & S

weight gain, fluid retention, moon face, increase adipose tissue in trunk, face, neck, thin extremities, muscle wasting, thin hair, easy to bruise, sex hormone alteration, glucose intolerance (high BS)

cushings diagnosis

elevated bs, low potassium, 24 hour urine for free cortisol

treatment of cushings DISEASE

removal of pituitary tumor, adrenalectomy if adrenal tumor, mitotane (med to suppress cortisol production),

treatment of cushiness SYNDROME

wean off steroids

addisons disease

adrenocortical insufficiency, primary and secondary

primary addisons disease

autoimmune

secondary addisons disease

from lack of pituitary ACTH

Manifestations of addisons diease

hypotension, vomiting, diarrhea, electrolyte imbalance, weakness, fatigue, anorexia, skin hyperpigmentation

risk of suddenly stopping steroid

severe hypotension and shock, will look like addisons disease

diagnosing addison's disease

low BG, electrolyte imbalance, metabolic acidosis, ACTH stimulation challenge test

ACTH stimulation challenge test

to find out if the problem is with the pituitary gland of the adrenal gland, measures the level of cortisol in your blood before and after an injection of synthetic ACTH. ACTH signals your adrenal glands to produce cortisol.

if adrenal glands are damaged ACTH stim test shows

output of cortisol blunted or non existent

care for addison's disease

replacement therapy with glucocorticosteroids and mineralcorticosteroids, manage underlying problem

shock

clinical syndrome characterized by inadequate tissue person that results in impaired cellular metabolism

types of shock

hypovolemic, distributive, cardiogenic

all shock effects

cardiac output

common to all types of shock

hypoperfusion, hypercoagulability, activation of the inflammatory process

MAP

normal 70-105, if not near normal=hypoxia

causes of hypovolemic shock

hemmorhagic, dehydration, burns, most common

hemorrhage

excessive loss of whole blood, external loss:GI hemorrhage, surgery, trauma
internal loss: hemothorax, dissecting AA

burns

shift of plasma from vascular to interstitial, direct evaporation loss, rule of nines

dehydration

nephrotic syndrome (leaky glomerolus), extreme third spacing

PNS

rest/homeostasis

SNS

fight or flight

distributive shock types

septic, anaphylactic

septic shock

systemic response to infection, may include SIRS and MODS, endotoxins bind with immune cells which initiate an inflammatory response causing severe vasodilatation and capillary permeability

anaphylactic shock

release of histamines leading to massive vasodilation and increased capillary permeability

manifest ions of anaphylactic shock

hives, laryngeal edema, bronchospasm, CV collapse, respiratory failure

cardiogenic shock

instability of the heart muscle to function adequately OR mechanical obstruction to or from the heart resulting in severe decrease of CO and decrease in tissue perfusion. MI, large PE, pericardial tamponade, tension pneumothorax

MI and cardiogenic shock

areas of necrotic tissue impairs the areas ability to contract, usually LV failure, decreased CO

CO=

volume x HR/min
normal 1500ml blood/min

PE and cardiogenic shock

increased workload RV>decrease blood to L side of heart >decreased CO

pericardial tamponade and cardiogenic shock

rapid increase in fluid in the pericardial sac which compresses myocardium impairing its ability to pump, decreasing CO

tension pneumothorax and cardiogenic shock

large amount of air in the pleural space which compresses the heart and great vessels > interrupts venous return to the heart > decreased CO

other causes of decreased CO

heart valve insufficiency (aortic stenosis), myocardial aneurysm, ruptured papillary muscles, ventricle rupture, cardiac dysrrhythmias

stages of shock

CO and tissue perfusion is impaired leading to initation, compensated stage, progressive stage, irreversible or refractory stage

stage 1 of shock, initiation

sub-clinical hypoperfusion, no S and S

stage 2 of shock, compensated stage

activation of SNS, decreased blood flow to kidneys, activates RAA system, decreased hydrostatic pressure in the BV causes fluid to move from the interstitial space into the intravascular space, the vasoconstriction keeps the organs perfused

SNS activation

blood flow to heart and brain is maintained, increased heart rate and cardiac output

RAA system

aldosterone causes and increase in NA and water reabsorption

stage 3 of shock, progressive shock

compensatory mechanisms are failing, vasoconstriction is prolonged causing decreased tissue perfusion, tissue hypoxia/anaerobic metabolosm/lactic acid build up, this is the shock cycle

stage 4 of shock, irreversible or refractory stage

compensation is ineffective, cellular death and MODS occurs, pooling and slugging of blood in microcirculation leads to clots, acidosis leading to increased capillary permeability

increased capillary permeability

fluid moves into interstitial (BP drops more, third spacing), hypotension/decreased coronary blood flow/CP arrest and cerebral ischemia

CNS and shock

most sensitive to changes in the supply of O2 and nutrients

CNS S&S of shock

restlessness, agitation, anxiety, unresponsiveness

cardiovascular response to shock

BP is initially maintained do to SNS response of vasoconstriction and increased contractility, and BP decreases systolic pressure will lower first, will see narrow pulse pressure, as shock continues decreased diastolic press will occur

respiratory response to shock

acid base imbalance due to increased CO2, decreased pH, as shock continues-metabolic wastes accumulate and cause generalized muscle weakness leading to shallow breathing and poor gas exchange

respiratory S&S of shock

increased rate and depth following by shallow

renal response to shock

hypo perfusion of kidneys leads to RAA system being activated, aldosterone being released leads to increased sodium and fluid reabsorption, auto regulation attempts to maintain GFR, once systemic BP is too low auto regulation stops, GFR decreases, Renal ischemia starts, decreased blood flow leads to ATN, ARF

renal S&S of shock

pre renal failure r/t hypovolemia, decreased UO and concentrated urine, increased BUN but creatinine may be normal, may lead to ATN

GI response to shock

SNS stimulation decreases the blood flow to GI tract, may lead to ileum, decreased tissue integrity, increased permeability of vessels, GI flora passes into blood stream bacteremia can lead to septicemia, liver is hypo perfused and has decreased ability to detoxify blood

GI S&S of shock

decreased bowel sounds, dissension, nausea, constipation

Hematologic system response to shock

DIC

DIC

sluggish blood in small vessels causes thrombosis, excessive clotting activates the fibrinolytic system, lysis of newly formed clots, depletes clotting factors and blood looses the ability to clot, stable clot does not form and breakdown of existing clots can lead to hemorrhage

treatment of DIC

heparin and platelets

S&S of DIC

bleeding

all forms of shock depress

macrophages which leads to a decreased ability to remove bacteria and endotoxins, a decreased ability to fight infection

endocrine systems response to shock (adrenal)

adrenal medulla-releases epinepherine and norepinepherine (SNS)
adrenal cortex-releases glucocoticoids and mineralcorticoids-aldosterone

endocrine systems response to shock (pituitary)

ADH released by posterior pituitary glad to retain water

integumentary system S&S of shock

pallor, cool moist skin
late:mottled or cyanotic

vasoactive substances

catecholamines, histamines, bradykinin, angiotensin

all forms of shock involve

decreased tissue perfusion

hypovolemic shock

initially urine osmolarity and specific gravity are increased, as shock continues the decrease

what I will see in hypovolemic shock

cool clammy skin, cyanotic, decreased urine output, decreased LOC, decreased LOC, decreased BP, increased HR

what I will see in cardiogenic shock

cool clammy skin, cyanotic, decreased urine output, decreased LOC, decreased LOC, EXTREMELY DECREASED BP, increased HR, JVD, chest pain

what I will see in anaphylactic shock

flushed warm skin, headache, dizziness, anxiety, disorientation, loss of consciousness, laryngeal adema, hoarse, dyspnea, stridor, bronchospasm, wheezing, decreased O2 sat, angioedema, hives

fecal/oral hepatitis spread

ECA

blood hepatits spread

BD

hep vaccines

A, B, C (B will help), D (B)

no hep vaccine for

E

Viral hepatitis

cannot live without host cell

bacterial hepatitis

can survive on its own

passive immunity

giving antibodies (breastfeeding)

active immunity

direct exposure or vaccine

antigen

protein marker on cell surface, tells body whether its self or foreign

antibody

immunoglobulin produced in response to a foreign body. play role in immune system. will attach to foreign body to destroy it

fulminant hepatitis

severe impairment of liver cells, necrosis, leading to liver failure

lobules

functional unit of liver

gallbladder function

receives, stores, concentrates bile

liver function

production of bile, bile salts, detoxification and metabolism of drugs, metabolism of alcohol, change ammonia to urea, bilirubin elimination, filtration of blood and removal of bacteria and particulate matter

bile needed for

digestion of fat and absorption of fat soluble vitamins

why do diabetics become hYPOgylcemic when they drink, cannot deal with glucose

the liver is busy detoxifying the alcohol

liver controls clotting factors

prothrombin and fibrinogen, dependent on vitamin K

Liver stores

ADEK, B12, and blood

ammonia is very

toxic to the body, especially the brain

bilirubin elimination

breakdown of RBC's, hemoglobin broken down into heme and globin. heme is converted to bilirubin

unconjugated/indirect bilirubin

before it gets to the liver

direct/conjugated bilirubin

after it gets to the liver, in bile, liver, stool

bilirubin in the intestines converts to urobilinogen/stercobilinogen

gives pt its color

clay stool=

liver problem

S&S of liver problems

clay stool, pruritis (bile salts), flu-like symptoms, bleeding problems, jaundice

jaundice-hemolytic/prehepatic

(not really liver disease), increased destruction of RBC's, liver can't handle it all, test will show UNCONJUGATED

reasons for increased RBC destruction (hemolysis)

autoimmune of transfusion hemolysis, sickle cell, septicemia, newborns, hemolytic anemia

intrahepatic jaundice

issue within the liver, liver disease. cirrhosis, hepatitis, cancer. blood test will show increased unconjugated or conjugated

posthepatic jaundice

obstructed outflow of bile from liver, blood test will show conjugated bilirubin

ascites

accumulation of fluid in the peritoneal space, sodium retention

portal hypertension

blockage of blood flow through the sinusoids to the hepatic veins and vena cava. causes increase in hydrostatic pressure in the portal venous system.

hepatic encephalopathy

r/t increased ammonia levels in the blood, mild confusion to deep coma, anxiety, euphoria, irritability, lack of coordination, factor hepaticus

fector hepaticus

sweet smelling breath

labs and tests for liver problems

viral antibodies for hepatitis, US, CT, Nuclear imagining, EDG, liver biopsy

icteric=

jaundice

preicteric phase

approx 2 weeks after exposure, GI issues, flu-like issues, rashes, itching, dark urine, light stool

icteric phase

5-10 days after initial symptoms, jaundiced skin, fever subsides, GI issues continue, hepatomegaly with tenderness. obstruction and inflammation of liver causes bile to be blocked from exiting liver

posticteric phase

4-6 months after initial symptoms, jaundice begins to subside, hepatomegaly continues, disappearance of jaundice does not mean fully recovered.

collaborative care for jaudice

interferon (boost immune system), ribavirin (antiviral), universal precautions

toxic hepatitis

liver injury or death following a toxic insult to the liver, drug induced, alcohol induced. eventually causes the build up of fatter acids (fatty liver)

treatment of idiopathic hepatitis

steroids and immunosuppressive drugs

cirrhosis-late clinical manifestations r/t dilation of BV

jaundice, palmar erythema, spider angioma, decreased body hair, itching, ecchymosis, edema, portal HTN, dysrhythmias, dyspna, esophageal varices, abd pain, anorexia, ascities, light colored stools, hepatic encephalopathy, asterixis, decreased clotting factors, thrombocytopenia, anemia, olgomenorrhea, testicular atrophy, gynecomastia, loss of libido

asterixis

flapping of hands (neuro problems)

cirrhosis def.

irreversible, progressive deterioration of liver, can be slowed, altered structure and function, fibrosis

alcoholic cirrhosis

fatty liver, can be reversible if ETOH is stopped before fibrosis occurs

postnecrotic cirrhosis

following viral, toxic, or autoimmune hepatitis

biliary cirrhosis

following viral, toxic, or autoimmune hepatitis

biliary hepatitis

due to chronic biliary obstruction and infections

cardiac hepatitis

from long time right sided heart failure

portal HTN

5-10mmHG, bands of fibrotic/scar tissue blocks the sinusoids and blood flow, portal vein to hepatic vein

treatment of portal HTN

TIPS (transjugular intrahepatic portosystemic shunt) stent places btw the high pressure portal vein and the low pressure hepatic vein, shunts some blood away from the portal system

esophageal varices

due to portal HTN, weakened/dilated veins in the esophagus due to backed up pressure from the portal vein, vary susceptible to bleeding, medical emergency

care for esophageal varices

sandostatin-IV med to promote vasoconstriction to reduce bleeding and portal HTN.
banding-variceal ligation-tiny rubber bands around varices
sclerosis-via EGD, injecting varicose with agent that causes vasoconstriction and sclerosing.
beta blockers
sengstaken-blakemore tube or minnesota tube-short term, applies pressure to stop bleeding

hepatic encephalopathy

brain problem r/t increased ammonia levels.
changes in LOC

treatment for high acid levels

lactulose, neomycin, oxazepam

nutrition therapy for cirrhosis

no protein during acute episodes

hepatorenal syndrome

pre renal failure due to liver problems. decreased GFR, ascites, edema

ascities

accumulation of fluid in the peritoneal space. low protein in the blood vasculature, meds: aldactone, lasix, albumin.
treatment: paracentesis, TIPS
nutrition: sodium restriction, fluid restriction

acute hepatic failure (fulminant)

medical emergency, severe, acute liver failure.
necrosis and loss of function, many systems involved, treatment is liver transplant

cause of acute hepatic failure

infections, drugs, toxins, hypo perfusion, GI surgeries, may be seen with or without previous problems

Portal HTN

r/t hydostatic pressure and fluid leakage. TIPS shunt

liver problems can lead to

clotting problems

worse case of liver failure

fulminant

cirrhosis prognosis

can stop progression, can not cure

end stage liver disease effects

all systems

alveoli

functional unit of lung

alveolar capillary membrane

where issues with gas exchange occur

pulmonary edema

oncotic/ostomic pressure (particles), hydostatic pressure (water), excess fluid in alveoli and further up, pink, frothy sputum.

3 main causes of pulmonary edema

issues with lymphatic system,issues with heart, injury to ac membrane

S & S of pulmonary edema

crackles, dyspnea, tachy, PND, aggitation, frothy pink sputum

VQ mismatch

vent, perfusion-same amount of air and blood should get to A/C membrane=match

increased vent, decreased perf

problem with blood flow (PE, vasculitis)

decreased vent, increased perf

problem with air. COPD, any airway blockage, asthma, mucus plug, bronchospasm, pulmonary edema

pulmonary embolism

pulmonary artery blockage, S&S: sudden onset chest pain, chest petichae, SOB, hemoptysis, tachycardia, tachypnea. Main cause: DVT
tx: heparin
dx: ddimer, spire cat scan

pulmonary HTN

primary: unknown
secondary to LV issues and others
tx: lung transplant
dx: ECHO, R sided heart cath, chest x-ray
anticoagulant won't help

acute respiratory failure

hypoxic-PaO2 less than 60 on 60% O2refractory

refractory

not responding

hypercapnic

elevated CO2, acidemia (pH less than 7.35) acidosis

hypoxic

decreased O2
tx: O2 ventimask (60%), non-rebreather (100%), ventilator, CPAP

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