Final Exam Flashcards
Name the 4 walls of the GI tract from innermost to outermost
- Mucosal layer
- Submucosal Layer
- Muscularis layer
- Serosal layer
What are the 3 subcomponents of the mucosal layer of the GI tract
- epithelium
- lamina propria (CT that contains capillaries and lacteals)
- muscularis mucosae (not important for motility, increases SA)
Describe the Submucosal layer
- connective tissue
- blood vessels, secretory glands and neurons
- submucosal plexus of Meissner’s plexus (post-ganglionic parasympathetic neurons)
Muscular layer
-inner muscle layer is circular and wraps tube
contractions narrow the tube
-outer layer contractions shorten and increase diameter of tube
Where is the myenteric plexus / Auerbachs plexus found
- muscluaris layer
- post ganglionic parasympathetic neurons
Parasymp and Symp in GI
- parasymp is stimulatory
- symp is inhibitory
What are the functions of saliva
- chemical digestion of CHO and some lipids
- lubrication of GI tract, aids in bolus formation
- enhances taste
- keeps mouth and teeth clean
How is saliva production stimulated
-parasymp, produces copious watery saliva
-smell
sour foods
local reflexes
Sjogren’s syndrome
- lymphocyte and plasma cells invade salivary and lacrimal glands
- dry mouth and eyes
- rheumatoid arthritis, lupus, scleroderma
What does the esophagus do?
moves bolus of food from mouth to stomach via peristalsis
Describe the cells in the esophagus
- proximal 1/3 is skeletal muscle, remainder is smooth muscle
- stratified squamous epithelium
- secretes mucus
Gastroesophageal Junction
abrupt transition from stratified epithelium to pseudo columnar epithelium (in stomach)
-lower esophageal sphincter is here
Lower Esophageal Sphincter
- anatomically distinct form surrounding smooth muscle
- allows ingested food into stomach and prevents stomach contents into esophagus
Gastroesophageal Reflux Disease (GERD)
- heartburn that occurs twice per week
- pain in upper/mid abdomen can radiate to chest, throat, shoulder, back
- made worse after eating large meals
- worse at night
- respiratory symptoms
GERD treatment
- stop smoking
- stop drinkin
- lose weight
- wear looser clothing
Barretts esophagus
- conversion of esophageal mucosa to intestinal mucosa after repeated exposure to gastric contents
- occurs in 10-15% ppl w/ GERD
- risk factor for esophageal cancer (adenocarcinoma)
Esophageal Cancer (adenocarcinoma)
- dysphagia and weight loss
- white males
- distal 1/3 of esophagus
Esophageal Cancer (squamous cell carcinoma)
-alcohol and smoking
-blacks
better prognosis
What makes pepsinogen
-chief or zymogenic cells
What do parietal cells do in the stomach
- make HCl
- make intrinsic factor
What does intrinsic factor do
-necessary for vitamin B12 absorption
Pernicious anemia
-lack of vitamin B12 from diet or intrinsic factor
Basic electrical rhythm of stomach
- generates peristaltic contractions
- pacemaker cells in longitudinal muscle layer generate contractions
- 3-5 contractions/minute
What is the role of the pyloric sphincter
- regulates outflow from stomach into duodenum
- only a small amount with each contraction 2-3mLs
Pepsinogen
- secreted by chief cells in the gastric pits
- active form is pepsin
- protease
- pepsin also activates more pepsin from pepsinogen
Hydrochloric acid HCl
- produced by parietal cells
- kills consumed microbes
- pH ranges 0-4 average 2
- low pH denatures proteins
- activates pepsin from pepsinogen
What simulates pepsinogen and HCl secretion?
- parasympathetic stimulation
- stomach distention
- protein
- histamine
What inhibits pepsinogen and HCl
increased duodenal activity
Acute gastritis
local irritation from alcohol, NSAIDs, bacterial endotoxins
- can include erosion of mucosa
- self limiting
Chronic gastritis
- no visible lesions
- chronic inflammatory changes that lead to atrophy of glandular epithelium
- increased risk for stomach cancer
Peptic Ulcer disease
-disruption of the mucosal barrier and exposure of underlying tissue to HCl and pepsin can result in ulceration of epithelium
Where does peptic ulcer disease occur?
-duodenal ulcers are 5X more common that gastric ulcers
Symptoms of peptic ulcer disease
-pain worse when empty stomach
-bleeding can occur
-
What is the goal of GERD and peptic ulcer Pharm
-reduce acid secretion, protect mucosa, prevent further damage and allow healing
H2 receptor blockers
- inhibits binding of histamine to H2 receptors
- suppresses HCl secretion
- decreases gastric acid secretion
H2 receptor side effects
-fatigue
-muscle pain
-GI upset,
CNS symptoms in older adults
-many drug interactions
Proton pump inhibitors
- prodrug, converted to active form in stomach
- binds to H+/K+ ATPase of parietal cells
- more effective/expensive than H2 blockers
- increased fracture risk
Carafate
- coating agent that bonds to protons, adheres to luminal surface of stomach
- not absorbed and doesn’t change pH
Pepto-bismol
- barrier forming
- stimulates bicarbonate and PGE2 secretion which inhibits H pylori growth
Cytotec
- coating agent
- abortion in pregnant
- not better
Symptoms of stomach cancer
- indigestion
- weight loss
- vomiting
Duodenum
- most important segment for digestion and absorption
- large SA
- produces bicarbonate that neutralizes gastric enzymes released into duodenum
Brush border Enzymes
membrane bound enzymes on the surface of absorptive cells in the small intestine
- perform final breakdown of consumed nutrients
- break down disaccharides into monosacs
Brunners gland
- produces alkaline mucus
- sensitive to sympathetic stimulation
- inhibits production of alkaline mucus
- can cause inappropriate lowering of duodenal pH and contribute to duodenal ulcers
Crypts of Leiberkuhn
- produce serous fluids that contains water and salts
- control of pancreatic secretions (secretin and CCK)
What stimulates the release of CCK by the small intestine
When fats are present in the duodenum
What causes release of bile salts into duodenum?
CCK stimulates contraction of the gall bladder which causes it to release bile salts
What is the purpose of bile salts?
emulsify fat
-increases the SA that pancreatic lipase can act
Segmenting contractions produced by the BER
- most important when the small intestine is moving a meal
- small segments contract and relax
- moves contents up and down within small intestine
- mixes content and maximizes contact with absorptive cells
- 12X/min in duodenum
Peristalsis
dominates between meals
-moves stuff in small intestine distally to avoid stasis of contents
Gastro-Ileal reflex
- when the stomach is active there is gastrin secretion, distention and gastric motility
- this causes distal small intestine to move contents to colon to make room for new
Absorption of protein in small intestine
- gastric, pancreatic, brush border enzymes perform digestion
- actively transport with Na+ or via facilitated diffusion
- absorbed into blood capillaries and transported to liver via portal system
Absorption of CHO in small intestine
- digestion via salivary, pancreatic, brush border enzymes
- actively transport with Na+ or via facilitated diffusion
- absorbed into blood capillaries and transported to liver via portal system
Absorption of fat in small intestine
- digestion primarily via pancreatic lipases, small contribution from salivary enzymes
- chylomicron synthesis in intestinal absorptive cells
- into lacteals and venous drainage into heart via lacteals
What is left in GI contents when it reaches the large intestine
-undigestible fiber, with some water and salts that were not absorbed in small intestine
Haustra
- puckers in the longitudinal muscle layer of the large intestine
- haustral churning is a major source of motility
Gastro-Colic reflex
- intense sustained contraction of 15-20cm of colon
- food in the stomach increases gastric motility and gastrin production
- this reflex stimulates mass movement in the colon
Defecation reflex
- stimulated by stretch of rectal smooth muscle
- afferents in rectal wall convey stretch info to sacral segments in SC
- parasymp efferents stimulate contraction of rectal smooth muscle
- internal anal sphincter must relax
- conscious control of relaxation of external sphincter then you poop
Irritable Bowel Syndrome
- chronic disorder characterized by abdominal pain and altered bowel habits in the absence of pathology
- more common in women (50% under 35 y/o)
IBS symptoms
- recurrent abdominal pain for at least 3 days/month for 3 months
- more or less bowel movements
- pooping makes you better
- any different type of stool
IBS treatment
- stress management
- avoid caffeine, lactose
- anti diarrhea’s
- tricyclic antidepressants
Inflammatory Bowel Disease
-Ulcerative colitis and Crohn disease
Crohn Disease
- may involve entire length of GI tract but proximal is rare
- ileum and cecum are common
- non specific granulomatous inflammatory process (skip lesions)
Crohn treatment
- avoid caffeine, spicy foods
- drugs
- corticosteroids
Ulcerative Colitis
- always originates in rectum, can progress proximally
- mucosal lesions that produce regions of ulceration and necrosis
Ulcerative colitis symptoms
- nausea, vomiting,
- abdominal pain
- rectal bleeding
- diarrhea
Rotovirus
-common in infants and kids-
fecal oral transmission
-poor absorption so diarrhea
Diverticular disease
- mucosal layer herniates through muscular layer forming a pouch
- low fiber diet is risk factor
Diverticulitis
-inflammation of diverticulum
Diarrhea treatment
-bananas
-rice
-applesauce
-toast
BRAT
What are the Renal functions (7)
- control extracellular fluid volume and osmolarity
- excrete metabolic wastes toxins and drugs
- synthesize hormones
- control ECF concentration of ions
- maintain the extracellular environment to keep cells functioning normally
How does the renal system regulate ECF volume
- controlling amount of NaCl in ECF
- amount of ingested NaCl that is retained vs excreted
How does the renal system regulate ECF osmolarity
- controls amount of ingested or synthesized water that is retained vs excreted
- add water ECF becomes dilute, remove water ECF becomes concentrated
Filtration
- the movement of water due to differences in hydrostatic pressure
- important in determining the movement of H2O between vascular and interstitial spaces
- not important in moving H2O between ICF and ECF
Osmosis
- important in moving H2O in and out of capillaries
- only factor that determines whether H2O moves into or out of cells
What is the average osmolarity of a human cell
300mOsm
-hypo= 300
If a cell is in a hypertonic solution it will ___
-shrink
If a cell is in a hypotonic solution it will ___
-swell
Lower than normal plasma
- pathology that prevents NA+ from being reabsorbed by the kidneys, individual loses more salt than water
- ECF gets smaller
- osmolatiry of ECF is lower
- cells swell
Where does urine collect in the kidney
- renal pelvis
- once urine reaches the renal pelvis it is not further modified
Nephron
-a tube lined with a single layer of epithelial cells that are sitting on a basement membrane
Artery flowing to the nephron is called the?
afferent arteriole
Glomerulus
-tufts of capillaries in bowman capsule
How much of the plasma in the afferent arteriole is filtered out into bowman space
- 20%
- the other 80% exits the nephron via the efferent arteriole
What does the loop of henle do?
communicates with the afferent arteriole to control blood flow
What is after the loop of henle
-distal convoluted tubule
Kidney filtration
- plasma into bowmans space is 180 liters per day
- looks like plasma in afferent arteriole
How is tubular fluid modified in the nephron
- tubular secretion
- tubular reabsorption
describe tubular secretion in the nephron
-the kidneys add solute to tubular fluid from the peritubular capillary network
Describe Tubular reabsorption in the nephron
- the movement of water and solute from the tubular fluid into the peritubular capillaries
- major process of modification of tubular fluid
What is different between systemic and renal capillaries
- starling forces (large hydrostatic pressure pushing plasma into bowman space that remains high along length of capillary)
- filtration barrier (glomerular caps are leaky
Transport maximum
- when transporters are saturated you get a further increase in solute concentration
- not all glucose appears in urine until transport maximum is reached
Plasma creatinine is proportional to _____
the number of function nephrons
What does the proximal nephron do?
-reabsorbs 67% of all filtered solutes and water except glucose and AA (b/c they are all reabsorbed)
In the proximal nephron reabsorptive functions are ______ homeostatic with respect to salt and water balance
- NOT
- 67% of water and solute will be reabsorbed regardless of ECF volume and osmolarity
What does the loop of Henle reabsorb
- 15% of filtered water
- 25% of filtered solute
What is preferential solute reabsorption
- when more solute than water is reabsorbed
- occurs in the LOH
Difference between ascending and descending limb
- ascending is impermeable to water
- decending is permeable to both salt and water
- this creates a gradient that allows for concentration of urine
Without ADH…..
-water is not reabsorbed in the distal nephron
What does ADH do?
the hormone that homeostatically regulates distal nephron water reabsorption
Excess water consumption does what to ECF osmolarity
- decreases
- which is sensed by osmo-receptors that stops production of ADH
What hormone controls distal nephron sodium reabsorption
-aldosterone, increases in this will increase sodium reabsorption in distal nephron
Normal pH levels
7.35-7.45
lower is acidosis
higher is alkalosis
What happens in ECF when [H+] is high
H+ moves into cells and K+ moves out causing hyperkalemia which depresses excitability
Acid
hydrogen ion donor
Base
hydrogen ion acceptor, takes hydrogen ions out of solution
Chemical buffer
minimizes pH changes in the presence of an acid or alkaline load very rapidly
What are the 3 systems that regulate plasma pH
- chemical buffers
- the lungs due to ability to control CO2
- kidneys due to ability to reabsorb HCO3 and secrete H+
Buffer systems
-have an acid component that will liberate H+ ions in solution when presented with an alkaline load and a base component that will remove H+ ions when challenged with an acid load
Henderson Hasselbeck equation
pH= pKa + log [base]/[acid]
Effectiveness of a buffer system
- based on the [ ] of the buffers, higher [ ] gives the buffer system a greater capacity to minimize pH changes
- the Ka, you want pKa near the desired pH
Metabolic acidosis
- pH is too low because [HCO3] is too low
- due to addition of fixed acids or loss of HCO3 like GI secretions
Metabolic acidosis response
- hyperventilate to decrease PCO2
- kidneys will reabsorb filtered HCO3 and secrete new HCO3 (takes hours to days)
Causes of metabolic acidosis
- production of fixed acids like lactate or ketoacids
- decreased ability of the kidney to reabsorb bicarbonate or secrete H+
- excessive loss of bicarbonate (diarrhea)
Symptoms of metabolic acidosis
hyperventilation
-decreased nervous system activity
Metabolic alkalosis
- pH is too high because HCO3 is too high
- due to addition of alkali or loss of H+ (vomiting_
Metabolic alkalosis response
-buffering by acid
-hypoventilation to increase PCO2
-kidneys will stop synthesizing HCO3 and stop reabsorbing HCO3
-
Causes of metabolic alkalosis
- much less common
- excessive alkali ingestion (antacids)
- chronic vomiting
- hypokalemia
Symptoms of metabolic alkalosis
- hypoventilation
- excitation of NS function (seizures)
Respiratory Acidosis
- pH is too low because PCO2 is too high
- caused by decrease in alveolar ventilation
Respiratory Acidosis response
- chemical buffers do not play role
- kidneys must reabsorb all filtered HCO3 and further synthesize new HCO3 to bring carbonic anhydrase equation back to the left
Causes of respiratory acidosis
- hypoventilation due to lung disease
- depression of respiratory centers
Symptoms of respiratory acidosis
- shortness of breath
- headache, blurred vision
Respiratory alkalosis
- pH is too high because PCO2 is too low
- not as common as resp. acidosis
Respiratory alkalosis response
-kidneys decrease HCO3 and stop synthesizing HCO3
Causes of respiratory alkalosis
- hyperventilation due to anxiety or panic attacks
- fever
- altitude
Symptoms of respiratory alkalosis
-hyperexcitability of CNS
Base excess/deficit
the amount of HCO3 that must be added or removed from blood to achieve a pH of 7.4
- positive = alkalosis
- negative = acidosis
Should protein/blood be present in urine
-no
What is the normal pH range for urine
5.5-8.0 or greater
What are the primary blood tests to evaluate kidney function
- blood urea nitrogen
- creatinine
What is GFR
- glomerular filtration rate
- indicates the number of functional nephrons in the kidney
Normal plasma creatinine levels
- 0 mg/dl
- if GFR is 50% of normal this value will double to 2.0
Blood urea nitrogen (BUN)
- normal value 8-20 mg/dl
- increase in BUN indicates decrease in GFR
- 2/3 of renal function can be lost before BUN increases
What factors can affect BUN
- increased dietary protein
- GI bleeding
- dehydration
What 3 ways can diuretics act?
- add non reabsorb able solute to tubular fluid to decrease gradient for distal reabsorption in distal nephron
- inhibit solute reabsorption which also decreases H20 reabsorption
- inhibit the release or action of ADH
Osmotic diuretic
- mannitol
- reduce intracellular H2O volume
- decrease intracranial pressure
Carbonic Anhydrase inhibitor
- acetazolamide
- inhibits NaHCO3 reabsorption
- can produce acidosis
- treat mountain sickness
Loop diuretics
- furosemide
- affect co transporter in loop of hence
- most potent diuretics
Thiazide diuretic
- inhibits NaCl transporter at luminal membrane
- hydrochlorothiazide
ADH antagonist
-treats hypertension/hyponatremia
Kidney stones
- damage can occur by urine stasis or increased pressure in urine tract
- Nephrolithiasis
Symptoms of kidney stones
-pain with location based on location of stone
Kidney stone treatment
- increase fluid intake
- pain relief
- avoid high oxalate foods
Glomerulonephritis
- inflammation and injury to glomeruli
- due to immune system attack
What are the symptoms of glomerulonephritis
- oliguiria
- proteinuria
- hematuiria
- azotemia
- hypertension
Nephrotic syndrome
- noninflammatory of golumerular cells causing gross proteinuria
- hyperlipidemia
Wilm’s tumor
- pediatric
- tumor of genitourinary tract
Causes of acute renal failure
- decreased renal blood flow from shock
- obstruction of urine outflow
- acute tubular necrosis
End Stage Renal Disease
Exercise concerns for patients with chronic kidney disease
- low CV fitness
- generalized weakness
- hypertension
What type of cells line the ureter and bladder?
transitional epithelium
Detrusor muscle
- when it contracts urine leaves the bladder
- internal urinary sphincter opens
- when bladder is released it prevents urine from leaving bladder
Female vs male urethra
-females are more prone to incontinence because there is less resistance to flow of urine
Excitatory input causing bladder emptying is ______
parasympathetic
Sympathetic input ______ bladder
relaxes
Pelvic nerve carries _____
sensory info from stretch receptors in bladder wlal
Pudendal nerve carries
sensory from external sphincter and pelvic muscles
Micturition reflex
- creates micturition waves that increase pressure and make you want to pee
- contraction of bladder activates stretch receptors which continues contraction
Anticholinergic
- block receptors that cause detrusor contraction
- decreased tone
Stress incontinence
- involuntary leakage on effort or exertion
- women under 60
Mixed incontinence
-involuntary leaking and urgency with effort
Overflow incontinence
-bladder too full beacuse it cannot empty
Functional incontinence
- cannot get to place to piss
- caused by mobility loss
UTI risk factors
- sexually active
- post menopausal
- obstruction
- diabetes
Washout phenomenon
-urine coming out flushes out bacteria
Pyelonephritis
ascending infection of urinary tract
-fever chills
What is the most common sign of bladder cancer?
painless hematuria
3 functions of the skin
- protection
- prevents loss of fluid
- synthesis of vitamin D
Stratum Germinativum
- deepest and single layer of keratinocytes
- cells travel upwards
Stratum Spinosum
2-4 layers thick and cells merge to form prickle cells
Stratum Granulosum
3-5 layers of flattened keratinocytes
-dark granules containing keratohyalin
Stratum Lucidum
-thin transparent layer found in hands and feet
Stratum Corneum
- multiple layers of dead keratinized cells
- 15-100 layers thick
Melanocyte
- dendritic cell producing melanin
- darker skin contains larger melanin with melanosomes
Langerhans cells
- antigen presenting dendritic cell from bone marrow
- important role in immune system
Merkel cells
- cutaneous sensation
- incresaed in hands for acute sensory perception
Dermis
connective tissue layer with primary nutrition source for epidermis
-made of immune cells blood vessels
Basement membrane zone
-interface between epidermis and dermis
Macule
small flat
- less than 1.0cm
- freckle
Patch
larger than 1.0 cm, change in color
-vitiligo
Papule
elevated superficial up to 1.0cm
-elevated nevis
Plaque
elevated superficial > 1.0cm
-expanding papule
Wheal
irregular transient superficial edema
-mosquito bite
Nodule
solid marble like >.5cm deeper and firmer than papule
Vesicle
up to 1.0 cm filled with serous fluid
-herpes
Bulla
> 1.0cm filled with serous fluid
-2nd degree burn
Pustula
pus filled
-acne
Ulcer
loss of epidermis and papillary dermis or subcutaneous tissue
-decubitous ulcer
Callus
hyperkeratotic plaque of skin
Corns
- small circumscribed keratinous thickenings of skin
- corn on toes hands
Albinism
-genetic disorder with partial absence of pigment in skin
Vitiligo
-sudden appearance of white macule on skin
Pruritus
-unpleasant sensation of itch leading to scratch
Xerosis
-composition of gland secretion and decrease sweating
Impetigo
- superficial bacteria caused by staph common in infants and kids
- small vesicle or large bulla
Herpes simplex
-infections of skin
Risk factors for skin ulcers
- impaired sensation
- skim moisture
- incontinence
Factors affecting wound healing
-nutritional status
blood flow and O2 delivery
-impaired immune response
