Unit 4

perfusion

heart failure

inability of the heart to pump blood to the body

causes: CAD, CHD, HTN, MI, valvular disease

effects:

• decreased CO (and SV) → increased HR, restructuring (dilated or hypertrophic cardiomyopathy)

• kidneys release renin → angiotensin I → angiotensin II (Na/H2O retention, vasoconstriction)

• kidneys release vasopressin (ADH) → H2O retention

primary insult: decreased CO → neurohormonal stimulation, ANP/BNP/norepinephrine/RAAS, nitric oxide inhibited

Left-sided HF: most common! cough, crackles, dyspnea, increased WOB (grunting, pursed lips, etc.), pulmonary edema

Right-side HF: less common! JVD, hepatojugular reflex, decreased urine output, peripheral edema, liver enlargement

elimination

liver

metabolic functions: produces bile, metabolizes hormones & drugs, synthesizes proteins/glucose/clotting factors, stores vitamins & minerals, changes ammonia → urea, converts fatty acids → ketones

blood supply: can store 500-1000 mL of blood, dual blood supply (venous/portal, and arterial)

• Kupffer cells: star-shaped cells that remove foreign particles & debris in the liver

diagnostics: AST, ALT, bilirubin, albumin, prothrombin time (PTT)

ascites: low albumin

jaundice: high bilirubin (>2/2.5 md/dL)

hepatic encephalopathy: high ammonia

exemplar(s)

alcohol-induced liver disease: leads to liver failure, esophageal varices, & kidney failure

1. fatty liver disease: “steatosis,” reversible

   1. sx: asymptomatic

2. alcoholic hepatitis: inflammation & necrosis of liver cells, occurs after abrupt increase in alcohol intake

   1. sx: liver tenderness, pain, anorexia, nausea, fever, jaundice, ascites

3. cirrhosis: irreversible damage, formation of nodules & compression of hepatic veins

alcohol metabolism: absorbed by stomach, metabolized by liver, end products (acetaldehyde & free radicals) → liver injury **women produce more acetaldehyde**

cirrhosis: end-stage chronic liver disease, functional tissue replaced by fibrous tissue

• causes: alcoholism, viral hepatitis, toxic drug reactions, biliary obstructions, NAFLD

• s/sx: weight loss, weakness, anorexia, diarrhea, hepatomegaly, jaundice, RUQ pain

• late manifestations: portal HTN, liver cell failure

  • causes of portal HTN: splenomegaly, ascites, esophageal varices, hemorrhoids, caput medusae

  • complications of portal HTN: ascites, splenomegaly, hepatic encephalopathy, portosystemic shunts (esophageal varices)

liver failure: 80-90% liver function lost before failure occurs

• manifestations: fetor hepaticus

• leads to: hematologic disorders, endocrine disorders, skin disorders, hepatorenal syndrome, hepatic encephalopathy

kidneys

functions: filter blood for reabsorption or excretion, elimination functions (regulate pH & electrolytes, uric acid/urea/drug elimination), endocrine functions (RAA mechanism, erythropoietin, vitamin D)

• nephrons: functional units of kidneys (~1,000,000 per kidney)

  • glomerulus: located btwn afferent & efferent arterioles, high pressure capillary filtration bed

    • Bowman capsule

• tubular components:

  • proximal convoluted tubule:

  • loop of Henle:

  • collecting duct:

  • distal convoluted tubule

• glomerular filtration: average GFR is 125 mL/min, filters plasma, regulated by afferent/efferent arterioles

urine concentration: depends on 1) osmolarity of interstitial fluids 2) ADH 3) action of ADH

diagnostics: casts, protein (0), specific gravity (1.005-1.025), GFR, BUN (8-20), creatinine (0.6-1.2)

exemplar(s)

acute kidney injury (AKI): possibly reversible

• prerenal: decreased renal blood flow (ex: shock, hypovolemia, HF)

• intrarenal: damage to nephrons (ex: diuretics, NSAIDs, antibiotics)

• postrenal: damage to ureter, bladder, etc. (ex: UTI, calculi, BPH, neurogenic bladder)

• azotemia: accumulation of nitrogenous wastes

• uremia:

phases:

1. onset: time from start of precipitating event → tubular injury (lasts hours-days)

2. oliguric: characterized by decreased GFR, lowest urine output, fluid retention, uremia, hyperkalemia (lasts 8-14 days)

3. diuretic: kidneys try to heal and increase urine output, tubule scarring/damage possible, elevated BUN, creatinine, K+, phosphate, and GFR

acute tubular necrosis (ATN): GFR does not improve w/ restoration of RBF, ischemia + nephrotoxin exposure = very high risk ATN, increased risk w/ dehydration

stress/cognition

• homeostasis: purposeful maintenance of stable internal environment

• allostasis: physiologic changes in the neuroendocrine, autonomic, & immune systems that occurs in response to real or perceived stressors

  • allostatic load: persistence of accumulation of the allostatic changes

  • allostatic overload: exaggerated pathophysiologic response to stress

Selye’s General Adaptation Syndrome

1. alarm stage: preparation for physiologic cascade

2. resistance stage: body attempts to restore homeostasis

3. exhaustion stage: stressor overwhelms body → damage OR body is able to rebound

• eustress: “good” stress

• distress: “bad” stress

hypothalamus → CRF → anterior pituitary gland → ACTH → adrenal cortex → cortisol

• locus coeruleus: area of the brainstem whose neurons produce norepinephrine

exemplar(s)

dementia: a decline in mental function that is severe enough to interfere with ADLs

• potentially reversible causes: drugs, emotional, metabolic, eyes & ears, normal pressure hydrocephalus, tumor, infection, anemia

• Alzheimer’s disease (AD): caused by tau plaques → amyloid tangles, irreversible

• vascular disease: d/t ischemic or hemorrhagic damage to brain

• Lewy bodies (Parkinson’s): accumulation of clumps of protein in the brain

Huntington disease (HD): genetic mutation of HTT gene (autosomal dominant - 50% transmission chance from affected parent)

• manifestations: appear in middle age (40s) in form of cognitive changes

Creutzfeldt-Jakob disease (CJD): infectious protein (prion) → encephalopathy

• manifestations: progressive dementia

• prognosis: fatal w/n 8 months

posttraumatic stress disorder (PTSD): caused by chronic activation of the stress response d/t experiencing significant traumatic event

1. intrusion: flashbacks in which traumatic event is relived

2. avoidance: emotional numbing that disrupts important personal relationships

3. hyperarousal: presence of increased irritability, difficulty w/ concentration, exaggerated startle reflex, increased vigilance, concern over safety