Physiology--> Exam 3 Ailments/questions

Front 1

The highest frequency of the rhythmic contraction in the small intestinge is determined by…

Back 1

Cells of Cajal. (Frequency of contraction, because we can only generate action potentials of the depolarization of the slow wave—if we can produce a contraction of each depolarization it will mean there are larger frequencies of contractions. We only get 1 contraction per each depolarization of the slow wave)

Front 2

frequency of rhythmic contraciotn of small intestine is determined by activity of …

Back 2

intestinal cells of cajal

Front 3

Motor neurons of the enteric nervous system control GI functions by action on

Back 3

intestinal smooth muscle cells, intestinal and vascular smooth muscle cells, secretory cells(exocrine), secretory cells endocrine

Front 4

the cell body of postganglionic parasympathetic neuron is located in...

Back 4

either in the myenteric plexus or submucosal plexus

Front 5

Achalasia

Back 5

Characteristics of achalasia:
a dilated, tortuous esophagus and the narrow lower end of esophagus deformity (bird's beak).

Usually caused by degeneration of the postganglionic inhibitory (NO/VIP) neurons in the myenteric plexus.
Characterized by abnormalities in peristalsis and in the tone of the LES:
Loss of a peristalsis of the esophagus
Loss of the LES relaxation in response to swallowing.
Elevated resting LES pressure
Functional obstruction and progressive esophageal dilation, stasis of food

Front 6

pirmary peristalsis in the esophagus is initiated by?

Back 6

vagal reflex. primary peristalsis initiated from the pharyngeal receptors. secondary peristalsis is initiated by strech of esophagus.

Front 7

the pressure in the body of the esophagus below the diaphragm between swallows is?

Back 7

greater than atmospheric pressure. slide 53

Front 8

The frequency of the rhythmic contraction in the small intestine is determined by activity of

Back 8

interstitial cells of cajal(pacemaker cells), neurons of enteric ns, ANS, mechanical stretch of the intestinal walls

Front 9

What maintains peristalsis in the stomach and small intestines during interdigestive state?

Back 9

MMC

Front 10

the H is secreted into the lumen of the stomach via the

Back 10

H+/K+ ATPase. H ion secreted by the potassium proton pump the na pump doesnt exist

Front 11

the most effective way to inhibit gastric acid secretion is to block:

Back 11

H, K-ATPase on the parietal cell. HCL secretion the most effective way to block it is through the proton pump

Front 12

frequency of rhythmic contraciotn of small intesting is determined by activity of

Back 12

intestinal cells of cajal, neurones of enteric nervous system, autonomic nervous system, mechanical stratch of the intestinal wall

Front 13

The highest frequency of the rhythmic contraction in the small intestine is determined by

Back 13

Cells of Cajal-because they are the initiator of depolarization. (Frequency of contraction, because we can only generate action potentials of the depolarization of the slow wave—if we can produce a contraction of each depolarization it will mean there are larger frequencies of contractions. We only get 1 contraction per each depolarization of the slow wave)

Front 14

Pyrosis (Heartburn)

Back 14

Gastric Acid Reflux
Low LES Tone
Foods and beverages that decrease LES tone
Chocolate, citrus juices, coffee, cola, tea, fatty meals, garlic, onions, peppermint, spices, tomato juices, ethanol
Weak 2° Peristalsis
↑ Gastric Pressure

Front 15

Diffuse Esophageal Spasm

Back 15

some swallows cause simultaneous contractions of the esophagus which may produce chest pain with radiation through to the back.

Front 16

Achalasia

Back 16

Characteristics of achalasia:
a dilated, tortuous esophagus and the narrow lower end of esophagus deformity (bird's beak).
Usually caused by degeneration of the postganglionic inhibitory (NO/VIP) neurons in the myenteric plexus.
Characterized by abnormalities in peristalsis and in the tone of the LES:
Loss of a peristalsis of the esophagus
Loss of the LES relaxation in response to swallowing.
Elevated resting LES pressure
Functional obstruction and progressive esophageal dilation, stasis of food

Front 17

Vomiting

Back 17

(Emesis) – protective reflex
Many stimuli (peripheral and central)
→ vomiting center: medulla →
→ nausea and retching →
→ autonomic discharge (salivation, sweating, pallor, dizziness, hyperventilation, variable heart beat)
→ REVERSE PERISTALSIS

Complications of vomiting
Loss of gastric contents: loss of fluid, H+ and ions (↓[K]; ↑pH)
Metabolic alkalosis and hypokalemia
Loss of small intestine content: additional loss of ions, fluid, bicarbonates, bile
Nutritional Deficiency
Ulceration
Weakening of UES and LES
Tooth Decay

Front 18

Hirschsprungs disease

Back 18

(a congenital absence of the enteric plexus in the distal colon)

Front 19

Diarrhea

Back 19

abnormally FAST stool transit (increased volume & liquidity)
Secretory
Osmotic
Inflammatory
Psychogenic

Front 20

Constipation

Back 20

abnormally SLOW stool transit (decreased volume & liquidity)
Dietary
Obstructive
Irregular bowel habits

Front 21

Peptic Ulcer Disease

Back 21

Acids and pepsin damage mucosal barrier and cause peptic ulcer disease
Damaged mucosal barrier → H+ leaks into the mucosa → cellular injury and death
H+ damages mucosal mast cells → stimulates histamine release → histamine acts on the mucosal capillaries →local ischemia, hypoxia, vascular stasis
Pepsin leaks into mucosa → plasma proteins leak into the gastric lumen → bleeding or vomiting

H. Pylori damages the mucosa by several mechanisms
produces NH4+ and various cytokines
Increases H+ secretion
Aspirin (NSAID) damages the mucosa
decreases mucosal production of prostaglandins (PGE2) by inhibiting cyclooxygenase (COX) and cause mucosal damage
PGs regulate secretion of mucus + HCO3- and maintain blood flow
Bile acids damage the mucosa
increase H+ leaks into the mucosa

Front 22

Nephropathies

Back 22

Negative charges on filtration barrier are reduced because of immunologic damage and inflammation
Proteinuria, albuminuria

Front 23

Hemorrhage

Back 23

can cause the renin release from granular cells of the kidney to set off a cascade to increase blood pressure by conserving Na+

Front 24

Which of the following arterial blood parameters indicate the respiratory acid base disorder?

Back 24

pH=7.6, pCO2=20mmHg, HCO3=16mEq/L =respiratory alkalosis.

Front 25

previous answer-- with or without compensation?

Back 25

using respiratory alkalosis formula plugging in the pCO2. it is chronic and is with compensation.

Front 26

Diabetes Insipidus

Back 26

causes:
neurogenic ADH deficiency typically due to head trauma, surgery, or neoplastic lesion
nephrogenic insensitivity to vasopressin
symptoms:
polyuria (copious urine production) lose water
polydipsia (extreme thirst)
treatment:
vasopressin analogue (desmopressin nasal spray) for neurogenic form.

Front 27

Syndrome of Inappropriate ADH Secretion

Back 27

Elevated plasma ADH levels
Retain water
Body fluids become hypoosmotic
Urine is very concentrated
Causes: infections and neoplasms of the brain, drugs, pulmonary disease, and some carcinomas