Module 4 Study Guide/Self-Test

respiratory

  • alveolar-capillary relation

    • Po2 is higher in alveoli than capillaries → O2 moves from alveoli to bloodstream for circulation

    • Pco2 is higher in capillaries than alveoli → CO2 moves from blood to alveoli for expiration

  • gas laws

    • gas moves down concentration gradients (high to low)

    • gas exchange depends on thickness of membrane, SA available, and gradients

  • lung diffusing capacity (DL)

    • how much gas the lungs can diffuse

    • accounts for diffusion coefficient, membrane SA, and membrane thickness, and time required for gas to combine with blood proteins

    • is affected by diseases

      • emphysema: decreases b/c alveoli are destroyed

      • fibrosis: membrane thickness is increased → DL decreases

      • anemia: less Hb → DL decreases

      • exercise: DL increases

  • perfusion-limited vs diffusion-limited gas exchange

    • perfusion-limited: limited by amount of blood/gas available to diffuse

      • diffusion can be increased by increasing blood flow

    • diffusion-limited: limited by ability of lungs to diffuse

      • e.g. fibrosis and emphysema: diffusion of O2 is restricted

  • lung volumes

    • TV: tidal V; how much air taken in/out in a normal breath

    • IRV: extra V that can be forcefully inhaled, e.g. in exercise

    • ERV: V that can be expired beyond a TV

    • RV: what’s left in the lungs after ERV

  • anatomic and physiologic dead space

    • anatomic: amt of space open (V of conducting airways); esophagus, nasal cavity, etc.

      • ~150mL

    • physiologic: anatomic + alveoli saturated with gas exchange, cannot currently participate

  • lung capacities

    • inspiratory capacity: TV + IRV

    • FRC: ERV + RV

    • VC or FVC: TV + IRV + ERV

    • TLC: TV + IRV + ERV + RV

    • FEV1: V that can be expired in the first second of a forced max. expiration

  • FEV1/FVC = 0.8 in healthy

    • how is this affected in obstructive lung disease? + an example

      • FEV1 reduced more than FVC → ratio decreases

      • e.g. asthma

    • how is this affected in restrictive lung disease? + an example

      • FEV and FVC are both reduced

      • e.g. fibrosis

  • mechanics of breathing

    • inhale: diaphragm pushes abdominal cavity down, intercostals lift ribcage up and out during active resp.

    • exhale usually passive

      • during exercise, abdominal ms. compress abdominal cavity and push diaphragm up, internal intercostals pull ribs down and in

  • surfactant: purpose and production

    • purpose: prevent alveoli from collapsing

    • production by type II alveolar cells

    • clin. point: neonatal respiratory distress syndrome: preemies don’t produce surfactant, have to be incubated and given cortisone injections to accelerate type II cell production

  • factors that change airway resistance

    • contraction/relaxation of bronchial smooth m.

    • lung V

    • viscosity/density of inspired gas

  • breathing cycle

    • at rest: alveolar P = atmospheric P, intrapleural P is (-), lung V is FRC

    • inspiration: ms. contract, thorax V increases → alveolar P decreases → pressure gradient causes air flow into lungs

      • lung V increases by 1 TV

    • expiration: alveolar P > atmospheric P → intrapleural P returns to resting value in passive expiration, lung V returns to FRC

  • asthma

    • airway constriction because inflammation because of irritant or autoimmune disease

    • decreased FVC, FEV1, and FEV1/FVC

    • increased FRC

  • COPD

    • obstructive, increased lung compliance, impaired expiration

    • combo of bronchitis and emphysema

    • pink puffer: 1* emphysema, normocapnia and mild hypoxemia

    • blue bloater: 1* bronchitis, hypercapnia and severe hypoxemia, cyanosis because no maintained alveolar ventilation

  • fibrosis

    • restrictive, decreased lung compliance, impaired inspiration

    • growth of fibrous material → loss of elasticity of lungs

    • decrease in all lung Vs, FEV1/FVC may be normal

  • bronchitis

    • inflammation of bronchi and bronchioles

  • forms of gases in solution

    • dissolved, carried by proteins, chemically modified

  • oxygen transport

    • dissolved and carried by proteins (Hb)

  • Hb O2 dissociation curve

  • CO2 transport

    • as HCO3-, mostly, because CO2 is harmful to body

    • some is carried by Hb

  • zones 1, 2, 3

    • 1: lowest blood flow because of gravity, alveolar > arterial > venous P

    • 2: medium blood flow, arterial > alveolar > venous P

    • 3: highest blood flow because of gravity, arterial > venous > alveolar P

  • regulation of pulmonary blood flow

    • hypoxic vasoconstriction: in hypoxia, vessels constrict to direct blood toward well-ventilated areas in lung

  • control of breathing

    • breathing occurs involuntarily, but hypo/hyperventilation can occur voluntarily

  • apneustic center: in lower pons

    • stimulates inspiration, produces deep prolonged inspiratory gasp

  • pneumotaxic center: in upper pons

    • inhibits respiration → regulates inspiratory V and respiratory rate

    • mnemonic: pneumotaxic = no inspiration

GI tract

  • structure and innervation

    • alimentary tract

    • parasym innerv. by vagus n. and pelvic splanchnic

    • sym innerv. by abdominal splanchnic ns

  • intrinsic innervation

    • sympathetic

    • parasympathetic

      • 2 plexuses: submucosal plexus of Meissner and myenteric plexus of Auerbach

  • GI motility

    • slow waves → segmental contractions → peristalsis is net movement from opening to opening

  • slow waves: occur regardless of APs, pacemakers, spontaneous from Cajal cells

  • spike waves: when stimulated and reach threshold, action potentials occur for contraction → strong contraction and peristalsis

    • stim by stretching, ACh, GI hormones, vagus/parasym stimulation

  • Ca2+ and muscle contraction

    • acts through calmodulin, not troponin C to regulate Ca and coordinate actin-myosin binding

  • tonic contraction: found in upper stomach, LES

  • propulsive peristalsis and mixing

    • mixing is no net movement, segmental contractions in 1-cm sections

    • peristalsis is 3-5 cm sections with net forward propulsion of bolus/chyme

  • Crohn’s disease: inflammation of GI tract → bloating, malabsorption

    • avoid high-fiber foods, greasy foods, alcohol, caffeine

    • autoimmune IBD

    • most commonly in large intestine

    • treated w/ antidiarrheal drugs, corticosteroids, immunomodulators, possible antibiotics

  • migrating myoelectric complex: contractions that occur every 90 minutes to clear tract of residual food

    • mediated by motilin

oral cavity

  • chewing, swallowing

    • chewing: initial mechanical breakdown and mixing of bolus with saliva for some chemical digestion and lubrication

    • swallowing propels food to esophagus to begin digestion

  • salivary glands

    • sympathetic innervation from salivatory nuclei (sup. and inf.), through CN VII and IX

    • parasympathetic innervation from

    • both innervs stimulate saliva production

  • mumps: myxovirus causes inflammation and white bumps on parotid gland

  • composition of saliva

    • some amylases, proteases, lipases, low Na and Cl, high K and HCO3-, hypotonic

esophagus

  • esophagus: tract from mouth to stomach

    • motility: peristalsis, closing of UES and LES

  • gastric reflux: LES doesn’t close properly → some stomach contents and HCl regurgitate up → irritation and burning

  • achalasia: LES cannot open completely → abnormal peristalsis because enteric NS has problem → food accumulates at upper esoph. → increased pressure

  • esophageal atresia: failure of LES to open (distal end is closed); middle part of esophagus is missing → vomiting

  • fistula: hole btwn esophagus and trachea → coughing

  • cancer: increased by opiate use, hot food/tea, smoke (irritation of mucosa)

  • hiatal hernias

    • sliding: fundus and part of stomach body come up through LES; regurgitation and heart burn

    • paraesophageal: fundus but no cardia comes up through LES; no regurgitation usually

      fundoplication: wrap fundus around stomach to prevent hernia

  • radiofrequency: burning valve to create scar tissue and tighten esoph. valve

stomach

  • hormones

    • G cells produce gastrin

      • increases HCl production and stimulates parietal cell growth

      • secreted by body and pylorus

      • important for protein digestion

      • oversecretion → risk for gastritis or ulcers

    • parietal cells produce HCl and intrinsic factor

      • HCl converts pepsinogen → pepsin

      • intrinsic factor carries vitB12 to ileum

    • chief cells produce pepsinogen

      • precursor to pepsin → digests proteins

    • ECL cells produce histamine and serotonin (paracrine hormones)

      • histamine increases HCl secretion (allergic reaction = irritation, acid is irritating)

      • serotonin indirectly controls HCl secretion (sneakily controls acid)

    • mucoid/goblet cells produce mucus

      • lubricate and protect stomach

    • D cells produce somatostatin and intrinsic factor

      • somatostatin inhibits other secretions (also secreted by pancreas)

        • from stomach: inhibits gastric hormone secretions

        • wants things to stay as they are, stops secretion

  • innervation: plexus of Meissner

  • mechanism of motility

    • circular and longitudinal contractions cause mixing and peristalsis

  • Zollinger-Ellison syndrome: pancreatic tumor creates gastrin-like product → increased HCl → gastritis

  • oxyntic glands: another name for parietal cells

  • gastric H+

    • mechanism

      • parietal cells: CO2 and H2O converted → H+ and HCO3-

        • cat. by carbonic anhydrase

      • H/K pump secretes H+ into stomach lumen with Cl- → product: HCl

        • inhibited by omeprazole

      • HCO3- is absorbed into bloodstream in exchange for Cl-, added to venous blood

    • stimulation of secretion: stimulated by gastrin

    • blockers: proton pump inhibitors (omeprazole), used to treat gastritis

  • gastritis: inflammation/irritation of stomach from xs H+ (HCl)

  • gastric ulcers: more severe than gastritis

    • no acid no ulcer

  • Menetrier’s disease

small intestine

  • function: digestion, absorption

  • motility

    • peristalsis: 3-5cm segments

    • segmental contractions: mixes/churns

  • duodenal ulcers: more common than gastric ulcers

  • duodenum hormones

    • I cells secrete CCK:

      • stimulates gallbladder contraction → secretion of bile

      • relaxes sphincter of Oddi to let duodenum receive pancreatic enzymes and bicarb.

      • stimulates pancreas for stimulation of enzymes and bicarb.

      • inhibits early gastric emptying when the chyme is fatty

    • S cells secrete secretin: controls HCl secretion from stomach

    • GIP stimulates release of insulin from pancreas in response to oral glucose

  • BER: basic electric rhythm: pacemaker again set by slow waves in intestine

  • ileocecal valve

    • separates small and large intestine

    • prevents backflow of feces into small intestine

  • villi: fingerlike projections, increase SA available for digestion and absorption

large intestine

  • function: absorption

  • Valsalva maneuver: increased intrathoracic pressure against closed glottis → urge to defecate

  • motility: slow waves, segmental contractions, peristalsis, MMC

  • segmental contractions

pancreas

  • function: produce digestive enzymes for small intestinal digestion (exocrine), produce insulin and glucagon (exocrine)

    • also produces bicarbonate for duodenum

  • secretion

    • stimulated by CCK

bile, gallbladder, liver

  • bile function: emulsify fats for digestion

  • bile formation:

    • hepatocytes form 1* bile acid from cholesterol → convert to 2* bile acids by bacteria → conjugated to bile salts → electrolytes and water get added → concentration

  • gallbladder contraction: stimulated by CCK and ACh

  • bilirubin: Hb taken from damaged/old RBCs in spleen

  • urobilinogen: becomes either converted to stercobilinogen → oxidized to stercobilin, or oxidized to urobilin

  • jaundice: yellowing of skin/eyes, signals issue with gallbladder or liver(buildup of bilirubin in skin)

  • gallstones: precipitation of salts or cholesterol because of imbalance in gallbladder

  • acute cholecystitis: inflammation of gallbladder wall

    • usually due to cystic duct obstruction by gallstone

  • liver function: detoxify and filter blood, store vitamins+iron+glycogen

  • liver pathologies: cirrhosis, hepatitis, hemochromatosis, Wilson’s disease

  • hepatitis: inflammation of liver

spleen

  • function: recycle damaged/old RBCs

    • removes Hb to become bilirubin

  • also stores emergency blood supply

  • produces and stores lymphocytes