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Pathophysiology Test #3

Terms in this set (187)

Pneumonia
inflammation of alveoli and bronchioles
Typical pneumonia
bacteria in the alveoli [lobar: affects an entire lobe of lung and broncho-pneumonia: patchy distribution over more than one lobe]
atypical pneumonia
viral and mycoplasma infections of the alveolar septum or interstitium (space between)
Tuberculosis mycobacterium tuberculosis hominis
Aerobic
Protective waxy capsule
Can stay alive in "suspended animation" for years
Initial TB infection
Macrophages begin a cell-mediated immune response
Takes 3 to 6 weeks to develop positive TB test
Results in a granulomatous lesion
or Ghon focus
Ghon focus contains
macrophages, T cells, inactive TB bacteria
Ghon complex
Nodules in lung tissue and lymph nodes.
Caseous necrosis inside nodules.
Calcium may deposit in the fatty area of necrosis.
Visible on x-rays
Primary TB
Cell-mediated hypersensitivity response
Granulomatous inflammatory response
Ghon complex
Healed dormant lesion
Secondary TB
Reinfection
Progressive or disseminated TB
Reactivated TB
Bronchogenic carcinoma
lung cancer, arises from epithelial cells lining the lugs
Manifestations of lung cancers
Changes in organ function (organ damage, inflammation, and failure)
Local effects of tumors (e.g., compression of nerves or veins, gastrointestinal obstruction)
Ectopic hormones secreted by tumor cells (paraneoplastic disorders)
Results in SIADH
Nonspecific signs of tissue breakdown (e.g., protein wasting, bone breakdown)
Hypoxemia
inadequate flow of O2 in the arterial blood
How much deoxygenated hemoglobin is required to be cyanotic?
greater than 5 g/dl
Impaired function of hypoxemia?
Agitated or combative behavior, euphoria, impaired judgment, convulsions, delirium, stupor, coma
Retinal hemorrhage
Hypotension and bradycardia
Activation of compensatory mechanisms
Hypercapnia
PCO2 > 50 mmHg
Hypercapnia leads to
respiratory acidosis
Pleuritis
Inflammation of the parietal pleura;
[Only the parietal pleura has pain receptors]
Pleural effusion
Abnormal collection of fluid in the pleural cavity
Hydrothorax fluid in the pleural cavity
serous fluid - often the result of HF
exudate fluid - contains inflammatory cells (contains lactate dehydrogenase &/or proteins
Empyema fluid in pleural cavity
pus
Chylothorax fluid in the pleural cavity
lymph
Hemothorax fluid in the pleural cavity
blood
Pneumothorax
air enters the pleural cavity
Spontaneous pneumothorax
air-filled blister on the lung ruptures
Traumatic pneumothorax
air enters through chest injuries [tension and open]
Open pneumothorax
air enters pleural cavity through the wound on inhalation and leaves on exhalation, rapid accumulation of pressure missing
Tension pneumothorax
air enters pleural cavity through wound on inhalation, cannot leave on exhalation
Atelectasis
Incomplete expansion of a lung or portion of a lung
Absorptive atelectasis
obstructed airway
Compression atelectasis
space occupying the lesion
Asthma
airway obstruction
Asthma inflammatory mediators
Airway inflammation
Increased mucociliary function
Edema
Epithelial injury
[Increased airway responsiveness
Bronchospasm Airflow limitation]
Extrinsic (atopic) asthma
Type 1 hypersensitivity: Cause acute response within 10 to 20 minutes
Bronchospasms
Increased mucus production
Airway inflammation causes late-phase response in 4 to 8 hours:
Mucosal edema
Impaired mucociliary function
Intrinsic (nonatopic) asthma
develops later in life; respiratory infections
COPD
can't get air out, emphysema and bronchitis
Emphysema
Characterized by loss of lung elasticity and abnormal enlargement of alveoli
[enlargement leads to hyperinflation]
Chronic bronchitis
Obstruction of small airways
Clinical diagnosis of chronic bronchitis
Chronic productive cough for 3 months in at least 2 consecutive years
Chronic irritation of airways [Increased number of mucous cells, goblet cells
Submucosal hypertrophy
Mucus hypersecretion in large airways]
Productive cough
Pink puffers
typically emphysema; Increase respiration to maintain oxygen levels
Dyspnea; increased ventilatory effort
Use accessory muscles; pursed-lip breathing
Blue bloaters
Cannot increase respiration enough to maintain oxygen levels
Cyanosis and polycythemia
Cor pulmonale
cystic fibrosis
recessive disorder in chloride transport proteins:
high concentrations of NaCl in sweat
less Na+ & H2O in respiratory mucus ad pancreatic secretions
(mucus is thicker = obstructs airway & pancreatic and biliary ducts)
interstitial lung disease
results in stiff and non compliant lungs (difficult to inflate) results in scar tissue
Primary pulmonary HTN
blood vessel walls thicken and constrict
Secondary pulmonary HTN
elevation of pulmonary venous pressure, increased pulmonary blood flow, hypoxemia, pulmonary vascular obstruction can lead to cor pulmonale
Cor pulmonale
right sided HF secondary to lung disease or pulmonary HTN
Acute Respiratory Distress Syndrome - ARDS
characterized by severe dyspnea of rapid onset, hypoxemia, & pulmonary infiltrates
Acute Lung Injury
less severe form of ARDS
How are ARDS and Acute lung injury differentiated?
by the extent of the hypoxemia
Hyaline membrane formation in ARDS
serves as barrier O2 cannot go through, ineffective gas exchange
Acute Respiratory failure includes what?
hypoxemic respiratory failure and hypercapnic/hypoxemic respiratory failure
Hypoxemic respiratory failure
due to failure of gas/exchange
mismatch of V/Q (COPD, severe PNA, atelectasis)
impaired diffusion (pulmonary edema, ALI/ARDS)
Hypercapnic/hypoxemic respiratory failure
due to inadequate ventilation (upper airway and obstruction muscle/chest wall injury)
Inflammatory Bowel Disease consists of ...
Ulcerative colitis and Crohns disease
Ulcerative colitis
chronic, infects the top mucosal layer,
starts @ the colon and works it way up ;
clinical manifestations - remission/exacerbation, very bad diarrhea
Crohns disease
not continuous, cobble stone appearace (granuloma), & transmural (which can develop fistulas)
clinical manifestations - ab pain/diarrhea, anemia
What are the two types of infectious enterocolitis?
viral infections - rota-virus & enteric adenovirus (kids), norovirus (all)
bacterial infections - ingestion, infection "food poisoning" more severe than viral
C. diff
gram positive spore forming bacillus; normal flora takes advantage of disruption of micro-flora environment can lead to pseudo-membranous colitis (life threatening)
E. coli
enterohemorrhagic, found in feces and contaminated milk of healthy dairy/beef cattle
Diverticulosis
asymptomatic diverticular disease
Diverticulitis
inflammatory stage of diverticulosis that can lead to peritonitis
Inflammatory diarrhea
presence of fever and bloody stool
Non inflammatory diarrhea
large-volume watery and non bloody diarrhea, periumbilical cramps
Osmotic diarrhea
non absorbable (a lot of) substances that draw water into the lumen; excessive motility, decrease transit time
1. short time bowel syndrome (not enough transit time), celiac disease, lactose intolerance, Mg, sulfate, phosphate
Secretory diarrhea
sick w/ a bug; excessive mucosal secretion of Cl or HCO3-,
i.e. fecal impaction
Types of constipation
primary and secondary
Primary constipation includes ...
normal transit - low fiber/fluid intake
slow transit - alteration in intestinal innervation (pace-maker, diabetes (gastroporesis)
pelvic floor dysfunction
Types of intestinal obstructions ...
mechanical - adhesion or hernias
functional - results from neurogenic or muscular impairment of peristalsis (ileus)
Functional intestinal obstructions
results from neurogenic or muscular impairment of peristalsis (ileus - loss of peristalic motor motility)
Mechanical intestinal obstructions
adhesion or hernias (femoral, inguinal, umbilical)
Peritonitis
inflammatory response of the serous membrane that lines the abdominal cavity (absent bowel sounds) [capillary permeable]
Malabsorption syndromes
interfere with nutrient absorption
Maldigestion
failure of the chemical processes of digestion (not breakdown the food)
Malabsorption
failure of intestinal mucosa to absorb (transport) the digested nutrients
Name the fat soluble vitamins
Vitamins D,A,K,E
Vitamin D deficiency
decreased calcium absorption, bone pain, osteoporosis, fractures
Vitamin A deficiency
nighttime blindness
Vitamin K deficiency
prolonged prothrombin time, purpura, petechiae (CLOTS) can lead to excessive bleeding
Vitamin E deficiency
testicular atrophy & neurologic defects in children
Pancreatic insufficiency
no lipase, amylase, trypsin
s/s fatty stools & weight loss due to pancreatic issues
Bile salt insufficiency
poor intestinal absorption of lipids
s/s fatty stools, diarrhea, loss of fat-soluble vitamins due to bile obstruction / liver disease
Lactose insufficiency
lactose not converting into monosaccharides due to genetics
Types of colorectal neoplasms
adenomatous polyps (beign neoplasms form mucosal epithelium of intestine) & colorectal cancer (adenocarcinoma)
The process of bile ...
the liver links unconjugated bilirubin to glucuronide which is then turned to conjugated bilirubin then bile
Jaundice
excessive bilirubin in blood (bilirubemia)
Four main causes of jaundice
excessive destruction of RBCs, impaired uptake of bilirubin by liver, decreased conjugation of bilirubin, obstruction of bile flow in canaliculi
Cholestasis
bile flow in the liver slows down; increased bile acids in blood and skin (pruritis)
Hepatitis
inflammation of the liver
Phases of viral hepatitis
incubation phase, prodromal (preicteric) phase, icteric phase, recovery phase
Incubation phase of viral hepatitis
varies, depending on the virus
Prodromal phase of viral hepatitis
prejaundice, begins 2 weeks after exposure, HIGHLY TRANSMISSIBLE, elevated AST, ALT levels
Icteric phase of viral hepatitis
actual illness (jaundice)
Recovery phase of viral hepatitis
resolution of jaundice
Alcoholic liver disease
causes damage to hepatocytes
Progression of alcoholic liver disease
steatosis, alcoholic hepatitis, & alcoholic cirrhosis
Steatosis
mild form of alcoholic liver disease & can be reversed
Alcoholic hepatitis
steatohepatitis, inflammation & degenaration/necrosis of hepatocytes
Alcoholis cirrhosis (fibrosis)
scar tissue & toxic effects, malnutrition,
Nonalcoholic fatty liver disease
associated with obesity, too many triglycerides
Biliary liver disease
cirrhosis begins in bile canaliculi and ducts
Cirrhosis
irreversible inflammatory fibrotic disease
Fibrosis is a consequence of what cells?
Kupffer
Cholecystitis
inflammation of the gall bladder
Cholangitis
inflammation of the bile ducts
Cholelithiasis
gallstone (cholesterol) formation
"fat, fair, female, fertile, and forty (familial)"
Pancreatitis
inflammation of the pancreas
Pancreatitis is associated with what two clinical disorders?
alcohol intake and cholelithiasis
Autodigestion enzymes
Enzymes that are leaked into pancreatic tissue due to injury or damage to pancreas
acute pancreatitis
resolves spontaneously
chronic pancreatitis
destroys acinar cells and the islets of Lagerhans
Cancer of the pancreas
mortality - approximately 95% within 12 months
RF - heavy cigarette, heavy alcohol use, family history of pancreatic cancer, & non type O group
Ductal adenocarcinoma
tumors of the exocrine cells in the duets
Tumors of the endocrine pancreas
rare; arise from islets of Langerhans, apudomas
initial s/s vague abdominal or midback pain & jaundice
Hormones of the stomach
gastrin, ghrelin, somatostatin
gastrin
released by stomach and doudenum, promotes contractions; stimulates gastric acid (created by parietal cells)
ghrelin
appetite stimulant signal; potent GH releasing activity, stimulatory effect on food intake and digestive function
somatostatin
inhibits acid and pepsinogen secretion and release of gastrin
hormones of the intestines
secretin, cholecytokinin (CKK), incretin
secretin
inhibits gastric secretion from duodenum
CKK
stimulates pancreatic enzyme secretion; important mediator for appetite [inhibits food intake and gastric emptying]
incretin
cause the release of insulin in response to carbohydrates
BMI: obesity
greater than equal to 30
BMI: overweight
greater than equal to 25
Four things to consider when assessing nutritional status
body weight, relative weight(actual/desirable), BMI, and percentage of body fat
peripheral obesity
(think pear) lower body obesity; gluteal-femoral, feminine, SQ obesity, less metabolically active than visceral
visceral obesity
(think apple) intra-abdominal, central or masculine obesity
increased risk for: inflammation, metabolic syndrome, DM 2, CV issues cardiovascular, HTN
Marasmus
mal-nutrition; too few calories and too little protein in diet
stunted growth, wrinkled skin, hypotonia (w/muscle)
Kwashiorkor
"diseased suffered by the displaced child"
adequate calories but too little protein in diet (affects visceral compartment more severely)
Cachexia
cytokine-induced malnutrition, associated w/ cancers and severely illed
Anorexia
loss of appetite
Nausea
ill-defined and unpleasant subjective sensation
common cause abdominal distention
vomiting
vomiting center can be activated by irritation from GI tract/abdominal organs, CNS stimulated by emotions/sights/sounds, vestibular apparatus motion sickness, chemo-receptor trigger zone (activated by chemical agent, drugs/toxins)
dysphagia
difficulty eating/swallowing; failure of the nerves to direct esophagus function (peristalsis)
achalasia
failure to relax, incomplete relaxation difficulty swallowing
esophageal diverticula
out-pouching of muscalaris layer trapped food that can lead to other complications
esophageal laceration
Mallory Weiss Syndrome, on penetrating mucosal tear of the GI esophageeal junction
hiatal hernia
protrusion or herniation of stomach through esophageal hiatus of the diaphragm
GERD
lower esophageal sphincter is weak/incompetent
Chronic inflammation, metaplasia, and dysplasia caused by GERD
Barretts esophagus
gastritis
inflammation of the stomach lining
acute gastritis
associated with H. pylori, NSIADs, drugs, chemicals (vague abdominal discomfort, epigasric tenderness, ad bleeding)
chronic gastritis
absence of grossly visible erosions and the presence of fhronic inflammaatory changes leads to atrophy of grandular epithelium
peptic ulcer disease
break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum
Zollinger-Ellison syndrome
peptic ulcer associated with gastrinomas and causes hypersecretion of gastric acid
very rare and malignant
Stress ulcer
peptic ulcer related to severe illness, multisystem organ failure, or major trauma
curling stress ulcer
related to burn injuries, trauma, ARDS, sepsis
decreased gastric motility (PNS shuts down)
cushing stress ulcer
related to head trauma, hypersecretion of gastric acid due to overstimulation of the vagus nerve
Mallory-Weiss syndrome
an esophageal laceration; non penetrating mucosal tear of the GI esophagela junction, near stomach & esophagus assoc. w/ upper GI bleed
hematemesis
bloody vomit (acute upper)
hematochezia
bloody stools (acute lower)
melena
tarry black stool (acute upper)
occult bleeding
not visible (chronic bleeds) need to get a guaiac test
_____________ drains into the anterior pituitary gland.
blood flow
_____________ feed the posterior pituitary gland.
nerve axons
Somatotropin
growth hormone
GH deficiency before puberty
dwarfism
GH deficiency after puberty
somatopause & tumors
GH excess before puberty
giagantism
GH excess after puberty
acromegaly
T3
stimulates metabolism, iodine required for formation
T4
inactive until converted into T3 in tissues
Primary hyperPTH
due to parathyroid adenoma
Secondary hyperPTH
another disease increasing the release of PTH
Manifestation of primary hyperPTH
hypercalcemia, hypercaliuria, hyperphospatauria, alkaline urine, kidney stones
Manifestations of secondary hyperPTH
excessive osteoclastic ~ bone fractures
hypoPTH
commonly caused by damge to PTH during thyroid surgery
manifestations of hypoPTH
hypocalcemia (Chvostek ad Trousseau sign)
mineralocorticoids
aldosterone
glucocorticoids
cortisol
adrenal androgens
DHEA
primary adrenal cortical insufficiency
addisons disease, TB major cause
manifestations of primary adrenal cortical insufficiency
mineralocorticoid/glucocorticoid deficiency and hyperpigmentation (too much ACTH)
secondary adrenal cortical insufficiency
rapid withdrawal of steroids; no hyperpigmentation
Cushing syndrome
adrenal cortical excess; HYPERCORTICOLISM, adrenal gland is broken
Cushing disease
tumor in pituitary; adrenal gland is functioning, excessive production of ACTH
Type 1A DM
autoimmune destruction of pancreatic cells
loss of beta cells
no insulin production
s/s of type 1A DM
hyperglycemia, hyperketonemia, absence of insulin = ketoss (metabolic acidosis)
type 2 DM
beta cell dysfunction and insulin resistance
Somogyi effect
hypoglycemic in the middle of the night then hyperglycemia in AM - adjust PM long acting insulin dosage
Dawm phenomenon
early morning glucose elevation R/T nocturnal GH stimulation
microvascular diabetic complications
diabetic - nephropathy, retinopathy, neuropathy
somatic diabetic neuropathy
diminished perception (vibration, pain, temperature)
hypersensitivty (light touch, severe "burning" pain)
autonomic diabetic neuropathy
defects in vasomotor and cardiac response, inability to empty bladder, impaired motility of the GI tract, ad sexual dysfunction
macrovascular diabetic complications
cardiovascular & cerebrovascular
hyperthyroidism
graves disease and diffuse goiter
graves disease
hyperthyroidism; autoimmune
triad associated with graves disease
exophthalmus, goiter, hyperthyroidism
also, preorbital myxedema
hashimotos thyroiditis
hypothyroidism; 10% of pregnancies result in subacute
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