Exam 2 Flashcards
Urinary system components and functions
- Kidneys: form urine
- Ureters: deliver urine to bladder
- Bladder: stores urine
- Urethra: expels urine from body
renal anatomy
- Kidneys are retroperitoneal and protected by lower ribs and adipose tissue
- Renal hilum: indented area that’s an entrance for renal artery, renal vein, ureter, nerves, lymphatics
External layers of renal anatomy: has connective tissue (superficial to deep)
- Renal fascia: anchors kidneys to other structures
- Adipose capsule: protects kidneys
- Renal capsule: adheres to kidney surface and protects spread of infection
Internal renal anatomy:
- Renal cortex: highly vascularized outer layer of kidneys with granular appearance
- Renal medulla: inner region used to creates concentrated urine
- Renal pyramids: urine-secreting apparatus and tubules
- Renal columns: anchors cortex
Cortical nephron:
- short loops of Henle that only extend to medulla’s outer region
- Renal corpuscle in outer portion of cortex
- Creates dilute urine with osmolarity similar to blood
- If hydrated ⇒ cortical dilutes water since there’s enough to spare
Juxtamedullary nephron:
- long loops of Henle that goes deep in medulla
- Renal corpuscle deep in cortex
- Receives blood from peritubular capillaries and vasa recta
- Ascending limb has thick and thin regions
- Enables kidneys to secrete very concentrated urine
- If dehydrated ⇒ juxtamedullary retains more water
What are the 2 parts of the renal corpuscle
- glomerulus
- glomerular (bowman’s) capsule
what is the glomerulus and what are the 3 layers of filtration?
- mass of capillaries that’s fed by afferent arteriole and drains to efferent arteriole
1. Glomerular endothelial cells: have fenestration (large pores) that are leaky = allowing for stuff from blood plasma to move in/out
2. Basement membrane: prevents filtration of larger proteins
3. Slit membrane between pedicels: prevents filtration of medium-sized proteins
what is the Glomerular (Bowman’s) Capsule and its function?
- has visceral layer of podocytes that wrap around capillaries
- Filtrate collected between visceral and parietal layers
Juxtaglomerular Apparatus
- region where ascending loop makes contact with afferent arteriole at macula densa
- arteriole walls have granular cells
- Regulates blood pressure in kidneys with help of autonomic nervous system
Renin-Angiotensin-Aldosterone System
Low salt levels ⇒ lowers blood volume b/c of inhibition of ADH secretion ⇒ pee more ⇒ less water reabsorbed in CT and more excreted in urine ⇒ lowered blood volume detected by granular cells that secrete renin to afferent arteriole ⇒ converts angiotensin → angiotensin I ⇒ angiotensin-converting enzyme (ACE) converts angiotensin I → angiotensin II ⇒ stimulates adrenal cortex to make aldosterone that stimulates K+ excretion and Na+ H2O reabsorption from CT ⇒ increases water reabsorption ⇒ increases blood volume and raises blood pressure
Glomerular Filtration + Secretion – Reabsorption = Excretion of Solute
- Glomerular filtration: blood plasma and dissolved substances get filtered in glomerular capsule
- Tubular secretion: happens along renal tubule and CT where substances and excess ions get secreted from peritubular capillaries to renal tubule to be excreted in urine
- Tubular reabsorption = happens along renal tubule and CT where water, ions, substances get reabsorbed from renal tubule to peritubular capillaries to be in blood
Glomerular filtration:
- Driven by blood pressure
- Opposed by capsular hydrostatic pressure and blood colloid osmotic pressure
- Capsular hydrostatic pressure: pressure of the fluid inside a capsule space
- Blood colloid osmotic pressure: amount of proteins in blood
- More proteins in blood than glomerulus space ⇒ opposes b/c it would want to drive things back into blood
- Water and small molecules move out of glomerulus
Glomerular filtration rate
- amount of filtrate formed by both kidneys each minute
- Homeostasis requires kidneys to maintain relatively constant GFR
- High GFR ⇒ substances pass too quickly and aren’t reabsorbed ⇒ higher BP
- Low GFR ⇒ almost all substances reabsorbed and some waste products not adequately excreted ⇒ lower BP
what are the 3 ways the kidneys are regulated?
- autoregulation (myogenic and tubuloglomerular)
- neural
- hormonal
2 types of autoregulation
- Myogenic mechanism:
- High BP ⇒ smooth muscle cells in afferent arterioles contract (b/c high BP means filtrate substances pass too fast and aren’t reabsorbed)
- Low BP ⇒ smooth muscle cells in afferent arteriole dilate (b/c low BP means almost all filtrate substances reabsorbed and barely any secreted)
- Tubuloglomerular feedback:
- High GFR ⇒ no reabsorption ⇒ macula densa inhibits release of nitric oxide (vasodilator) ⇒ afferent arterioles constrict
Neural regulation
strong sympathetic stimulation ⇒ afferent arterioles constrict ⇒ reduced urine output ⇒ more blood available for other organs
Hormonal regulation
- High GFR?
- High BP?
-High GFR ⇒ angiotensin II constrict afferent and efferent arterioles ⇒ decreases GFR
- High BP ⇒ Atrial natriuretic peptide (ANP): released in response to stretch of cardiac atria when BP is too high and relaxes mesangial cells in glomerulus ⇒ increases capillary surface area ⇒ low BP
Angiotensin II:
- stimulates adrenal cortex to make aldosterone
- constricts afferent and efferent arterioles
Aldosterone
stimulates K+ excretion and Na+ reabsorption which also reabsorbs H2O because it follows Na+
ADH
stimulates insertion of aquaporins in CD ⇒ increases H2O reabsorption to peritubular capillaries
ANP: atrial natriuretic peptide
during High BP ⇒ inhibits secretion of aldosterone and ADH ⇒ suppresses reabsorption of Na+ and H2O in PCT and CD ⇒ increases excretion of Na+ in urine ⇒ increases urine output ⇒ decreases blood volume and BP
PTH
stimulates opening of Ca2+ channels in DCT ⇒ increases reabsorption of Ca2+
Renin
converts angiotensinogen → angiotensin I
Angiotensin-converting enzyme (ACE)
converts angiotensin I → angiotensin II
Formation of Dilute urine:
- Osmolarity (solute concentration) in tubule when urine is dilute:
- Increases in descending limb
- Decreases in ascending limb
- Decreases more in CD - Thick ascending limb:
- Symporters reabsorb Na+, K+, Cl- ⇒ solutes move out of tubules ⇒ low osmolarity
- Low water permeability = solutes leave and water stays - DCT and CD:
- Both permeable to water upon ADH release
- Low permeability in absence of ADH
Formation of Concentrated urine
- Osmotic gradient created by countercurrent multiplier: medulla osmolarity increases as solutes are pumped out of ascending limb = maintains hypertonicity of medulla for solutes to go out of tubule during descending limb
- With ADH = CD become permeable to water = water moves out and urine becomes more concentrated
- Movement of water carries urea to medulla ⇒ increases osmolarity
where does countercurrent exchange happen?
Loop of Henle of the Juxtamedullary nephron
steps to countercurrent exchange
- Descending limb: permeable to water = water move down osmotic gradient out of tubule to interstitial fluid in medulla because of hypertonicity of medulla
- Medulla already had high hypertonicity b/c it has lots of solutes stuck in medulla capillaries not reabsorbing solutes very well - Ascending limb: impermeable to water but permeable to solutes = sodium and chloride symporters move ions from tubule to interstitial fluid in medulla = increases hypertonicity of medulla further
- DCT & CT: upon ADH release, aquaporin channels will be introduced to DCT & CT = water reabsorption = formation of concentrated urine
- Urea recycling: contributes to hypertonicity of renal medulla by reabsorbed in CD and secreted into nephron loop = goes through nephron loop that’s impermeable so it can’t get out of filtrate until it’s in CD = recycles urea and increase tonicity of interstitial fluid in medulla
urea recycling steps
- PCT: urea is reabsorbed with water, but there’s more water being reabsorbed than urea ⇒ urea concentration in the tubule than in the blood.
- Descending limb: there’s higher concentration of urea in interstitium of medulla already ⇒ urea concentration in tubule is less than urea concentration outside ⇒ high concentration of urea in interstitial medulla moves back into tubules
- Ascending limb: urea is impermeable so it stays in tubule
- DCT and CT: there’s ADH that increases water reabsorption and water already moves out of tubule because surrounding osmolarity in interstitium already high due to some urea and lots of other solutes ⇒ still have lots of urea in tubule due to when urea was secreted back into tubule in descending limb ⇒ concentration of urea in tubule in CT is greater than in interstitium ⇒ some of urea leaves tubule and goes out to interstitium ⇒ urea gets secreted back into descending limb’s bottom of loop ⇒ urea makes its way back up ascending limb to DCT and CT to do process again ⇒ urea recycled
Acute renal failure
- failure of kidneys’ abilities to excrete wastes, regulate blood volume, pH, and electrolytes
- caused by inflammation of tubules or kidney ischemia
- Signs: rise in blood creatinine and decrease in renal plasma clearance of creatinine
Glomerulonephritis
- inflammation of glomeruli
- Autoimmune attack against glomerular capillary basement membranes ⇒ leakage of protein to urine ⇒ decreased colloid osmotic pressure ⇒ edema
Renal insufficiency
- nephrons destroyed
- Results in salt, H2O retention and uremia along with high plasma H+ and K+ ⇒ coma
Polycystic kidney disease (PKD)
inherited disorder where clusters of fluid-filled sacs develop in kidneys ⇒ kidneys enlarge and lose function over time
What are the parts to Fluid compartments and fluid homeostasis
- plasma membrane of cells
- blood vessel walls
- capillary walls
- filtration, reabsorption, diffusion, osmosis
- level of aerobic respiration determines volume of metabolic water formed because…
- when water loss > water gain = dehydration ==> increased thirst
- elimination of excess body water occurs via urine production
Plasma membrane of cells
separates intracellular fluid from interstitial fluid
Blood vessel walls
divide interstitial fluid from blood plasma
Capillary walls
thin enough to allow exchange of water and solutes between blood plasma and interstitial fluid
Filtration, reabsorption, diffusion, osmosis:
- allows continuous exchange of water and solutes among body fluid compartments
1. Balance of inorganic compounds that dissociate into ions (electrolytes) closely related to fluid balance- Low electrolytes = less water reabsorption because water follows solutes (electrolytes)
- Body gains water by ingestion and metabolic synthesis
- When cells use energy they produce metabolic water
- Body loses water via urination, perspiration, exhalation, and in feces
- Water vapor is in air exhaled out
- Low electrolytes = less water reabsorption because water follows solutes (electrolytes)
Level of aerobic respiration determines volume of metabolic water formed b/c…
Amt of water formed is directly proportional to amt of ATP produced
Elimination of excess body water occurs via urine production. What are the 2 main solutes and the 3 main hormones controlling them?
- Amt of urinary salt loss is main factor in determining body fluid volume
- 2 main solutes in urine: sodium ions (Na+) and chloride ions (Cl-) that both flow together to keep electrochemical charge balance
- Wherever solutes go = water follows
- 3 major hormones that control renal Na+ and Cl- (controls water through solute movement): angiotensin II, Aldosterone, ANP
ADH and its impact on diabetes insipidus
- CD is last stop in urine formation
- CD impermeable to NaCl but permeable to water
- Influenced by hypertonicity of interstitial space = water leaves via osmosis is able
- Permeability to water depends on number of aquaporin channels in cells of CD
- Availability of aquaporins determined by ADH
- ADH stimulates aquaporin channels
- Diabetes insipidus: urine is dilute, characterized by polyuria, thirst, and polydipsia
- 2 major types…
- Central diabetes insipidus: inadequate secretion of ADH
- Nephrogenic diabetes insipidus: inability of kidneys to respond to ADH (Can be caused by genetic defects in aquaporin channels or ADH receptors)
- 2 major types…
Atrial Natriuretic Peptide (ANP)
- Increased blood volume ⇒ increased ANP release from atria of heart because during high blood volume, the atria’s walls stretch more ⇒ stimulates kidneys to excrete more salt ⇒ excretes more water ⇒ decreases blood volume and blood pressure
- inhibits secretion of aldosterone and ADH ⇒ suppresses reabsorption of Na+ and H2O in PCT and CD ⇒ increases excretion of Na+ in urine ⇒ increases urine output ⇒ decreases blood volume and BP - Decrease in blood volume ⇒ decrease in ANP release from atria of heart because atrias feel less stretch with low blood volume
- b/c ANP also relaxes mesangial cells in glomerulus ⇒ increases capillary surface area ⇒ increases GFR (if you decrease ANP you decrease relaxation = you stop it from further increasing capillary surfaces = stops it from decreasing GFR)
B-Type Natriuretic Peptide (BNP)
Increased blood volume ⇒ increased BNP release from ventricles ⇒ promotes diuresis
functions of electrolytes (ions in watery solution)
- Control osmosis of water between fluid compartments
- Helps maintain acid-base balance
- Carries electrical current and their charges
- serve as cofactors
Sodium
- most abundant cation in extracellular fluid
- Used for impulse transmission, muscle contraction, fluid, and electrolyte balance
- Controlled by aldosterone, ADH, ANP
Chloride
- major extracellular anion
- Helps regulate osmotic pressure between compartments
- Forms HCl in stomach
- Controlled by aldosterone
Potassium
- most abundant cation in intracellular fluid
- Involved in fluid volume, impulse conduction, muscle contraction, regulating pH
- Mineralocorticoids (mainly aldosterone) regulates plasma levels
Bicarbonate
- important plasma ion
- Major member of plasma acid-base buffer system
- Kidneys reabsorb or secrete it for final acid-base balance
Magnesium
- intracellular cation
- Activates enzyme involved in carbohydrate and protein metabolism
- Used in myocardial function, transmission in CNS, and operation of sodium pump
Calcium
- most abundant mineral in body
- Structural component of bones and teeth
- Used for blood coagulation, neurotransmitter release, muscle tone, excitability of nerves and muscles
- Regulated by PTH
Phosphate
- occurs in calcium phosphate salt
- Used in buffer system
- Regulated by PTH and calcitriol
Protein buffer system
- most abundant in intracellular fluid and blood plasma
- pH rises ⇒ COOH group dissociates ⇒ acts like acid
- pH falls ⇒ free amino group dissociates ⇒ acts like base
Carbonic acid-bicarbonate buffer system
- based on bicarbonate ion (HCO3-) acting as weak base and carbonic acid (H2CO3) acting as weak acid
- pH rises ⇒ H2CO3 can be broken down to hydrogen H+ and HCO3- bicarbonate ion (weak base)
- pH falls ⇒ HCO3- combines with excess H+ ⇒ makes carbonic acid H2CO3 ⇒ H2CO3 broken down to carbon dioxide and water with carbonic anhydrase ⇒ carbon dioxide exhaled out
Phosphate buffer system
- dihydrogen phosphate H2PO4- (weak acid) and monohydrogen phosphate HPO4-2 (weak base) used
- pH rises ⇒ hydrogen H+ combines with monohydrogen phosphate (weak base) to form dihydrogen phosphate (weak acid)
- pH falls ⇒ hydroxide OH- combines with dihydrogen phosphate (weak acid) to form water and monohydrogen phosphate (weak base)
Exhalation of carbon dioxide
- CO2 mixes with water in blood to form carbonic acid H2CO3 and H2CO3 can be broken down to water and carbon dioxide via carbonic anhydrase
- Exhaling CO2 ⇒ less acid production ⇒ rise in pH
- Retaining CO2 ⇒ more acid production ⇒ drop in pH
Kidney excretion of H+
- renal tubules secrete H+ into urine and reabsorb HCO3- so it’s not lost in urine
- Excreting H+ in urine removes nonvolatile acids
- PCT and CD secrete H+ to tubular fluid to be excreted while some buffered by HPO4-2 and NH3 (buffers excreted in urine)
Acidosis
blood pH below 7.35
Alkalosis
blood pH above 7.45
Respiratory acid-base imbalances
related to carbon dioxide levels in blood (fixed with renal)
Respiratory acidosis
- blood pH drops due to excessive retention of CO2 ⇒ excess H2CO3
- Kidneys compensate by excreting more protons (H+) and increasing reabsorption of bicarbonate ions
Respiratory alkalosis
- blood pH rises due to excessive loss of CO2 via hyperventilation
- Kidneys compensate for respiratory alkalosis by excreting more bicarbonate and increasing reabsorption of protons (H+)
Metabolic acid-base imbalances
related to bicarbonate (HCO3–) levels in blood (fixed with respiratory)
Metabolic acidosis:
- arterial blood levels of HCO3- falls
- Lungs compensate by hyperventilation ⇒ increases loss of CO2 ⇒ less carbonic acid formation ⇒ less acidity
Metabolic alkalosis:
- arterial blood levels of HCO3- rises
- Lungs compensate by hypoventilation ⇒ retention of CO2 ⇒ more carbonic acid formation ⇒ less acidity
Diuretics
- used to control BP and relieve edema (fluid accumulation)
- Diuretics increase urine volume, decreasing blood volume and interstitial fluid volume
3 Types of diuretics
- Loop diuretics: most powerful, inhibits salt transport out of ascending loop ⇒ inhibits water reabsorption ⇒ dilutes urine
- Osmotic diuretics: reduce reabsorption of water by adding extra solutes to filtrate ⇒ water stays with solutes ⇒ less water reabsorption ⇒ dilutes urine
- Potassium-sparing diuretics: aldosterone receptor antagonist ⇒ blocks reabsorption of Na+ and secretion of K+ ⇒ less water reabsorption ⇒ dilutes urine
PAH and inulin clearance
diagnosis nephritis or renal insufficiency
Urinary albumin excretion rate test
detects above-normal albumin excretion– microalbuminuria ⇒ signifies renal damage due to hypertension or diabetes
Proteinuria
overexcretion of proteins signifying nephrotic syndrome
Layers of the GI tract (outside to inside layers)
- Muscularis:
- Outside to inside: longitudinal muscle → circular muscle
- Submucosa
- Mucosa:
- Outside to inside: muscularis mucosa → lamina propria → epithelium
Mouth parts: Hard palate, soft palate, uvula, and lingual frenulum
- Hard palate: bony, forms most of mouth roof
- Soft palate: muscular, forms rest of mouth’s roof
- Uvula: prevents swallowed food from entering nasal cavity
- Lingual frenulum: limits movement of tongue posteriorly
Tongue: forms floor of oral cavity
- Composed of skeletal muscle covered with mucous membrane
- Functions: chewing, swallowing, and speech
- Upper and later surfaces covered with papillae (some containing taste buds that serve as receptors for taste and presence of food in mouth)
- Shapes chewed and lubricated food and moves it to back of mouth cavity
- Rises against palate and closes nasopharynx when swallowing
Pharynx: funnel shaped tube that extends from internal nares to esophagus
Composed of skeletal muscle lined with mucous membrane to make food go down further esophagus
Esophagus: collapsible, muscular tube that lies posterior to trachea and connects pharynx to stomach
- Collapses on itself when not swallowing
- Goal: get food from pharynx and transfer it to stomach
- Walls (outside lumen to inside):
- Mucosa: nonkeratinized stratified squamous epithelium
- Muscularis: circular layer
- Muscularis: longitudinal layer
Pancreas: gland that lies posterior to stomach
- Produces enzymes that digest carbs, proteins, fats, nucleic acids
- Produces sodium bicarbonate which buffers stomach acid
- Empties its contents to duodenum
- Delivers pancreatic juices to duodenum via pancreatic duct to assist absorption
Stomach: J-shaped enlargement of GI tract
- Mixes saliva, food, gastric juices ⇒ forms chyme
- Serves as reservoir for food before releasing it to small intestine
- Secretes gastric juice (contains HCl, pepsin, intrinsic factor, gastric lipase)
- Gastric glands and cell types surface mucous cells, mucous neck cells, parietal cells, chief cells, G-cells
- Has Muscularis: mixing waves that churns and physically breaks down food and mixes it with gastric juices ⇒ forms chyme to go through pyloric sphincter
- Has Pyloric sphincter: opens to pass chyme to duodenum and prevents backflow of chyme from duodenum to stomach
Cephalic phase
- Happens at sight, smell, taste, or thoughts of food that secretes saliva for food
- Stimulates gastric secretion and motility by activating parietal and G-cells to make stomach ready to receive food
Gastric phase
- Caused by stretching stomach and stimulating receptors
- Most gastric acid secretion happens during stage to make chyme in stomach
Intestinal phase
- Chyme arrives in small intestine
- Inhibits gastric secretion and emptying (b/c food is already out so no need for stomach movement) by release of secretin and cholecystokinin (CCK)
Phases of Digestion
- Cephalic Phase
- Gastric Phase
- Intestinal Phase
Liver
- Stores glycogen and fat
- Regulates blood sugar by removing glucose and storing it as glycogen and triglycerides
- Can also break down glycogen ⇒ increases blood sugar and make glucose from amino acids (too much protein = excess is broken down = forms glucose)
- Produces plasma proteins
- Detoxifies blood
- Production of bile that leads to emulsification (break down) of fat globule to small droplets ⇒ more surface area for enzyme lipase to break it down to small fats
- Produces some bilirubin: toxic product made from RBC breakdown and excreted in feces, urine, and bile
Gallbladder
stores, concentrates, and releases bile to duodenum via common bile duct
Function of the small intestines including intestinal juices and mechanical digestion
1.Main functions: major site of digestion and absorption of nutrients and water in GI tract
- Segmentations mix chyme with digestive juices (secreted by pancreas) and brings food into contact with mucosa for absorption via peristalsis that propels chyme
- Completes digestion of carbs, proteins, lipids, nucleic acids
- Absorbs 90% of nutrients and water that passes through
2. Has circular folds that increase surface area for digestion and absorption
3. Mechanical digestion:
- Segmentation: alternating contractions of circular smooth muscle fibers that mixes chyme with digestive juices and brings food to contact with mucosa for absorption
- Migrating motility complex (MMC): waves of contraction and relaxation of circular and longitudinal smooth muscle fibers that moves chyme towards ileocecal sphincter
4. Chemical digestion: digestion of carbs, proteins, lipids, and nucleic acids
Summary of Digestive Activities in the Pancreas, Liver, Gallbladder, and Small Intestine
- Pancreas: delivers pancreatic juice to duodenum via pancreatic duct to assist in absorption
- Liver: produces bile for emulsification and absorption of lipids
- Gallbladder: stores, concentrates, and delivers bile to duodenum via common bile duct
- Small intestine: major site for digestion and absorption of nutrients and water in GI tract
Summary of Digestive Enzymes
- Saliva
- Gastric Juices
Saliva
- Salivary amylase: breaks down starches to make maltose, maltotriose, and a-dextrins
- Lingual lipase: breaks down triglycerides and other lipids to make fatty acids and diglycerides
Gastric juice
- Pepsin (activated from pepsinogen by pepsin and HCl): breaks down proteins to make peptides
- Gastric lipase: breaks down triglycerides to make fatty acids and monoglycerides
Functions of colon
- Haustral churning (condenses and packs food to turn it to proper feces), peristalsis, mass peristalsis driving contents of colon to rectum
- Already absorbed things needed from content atp - Bacteria in colon converts proteins to amino acids, breaks down amino acids, and produces some VitB
- Absorption of some water, ions, and vitamins
- Forms feces and defecation
Functions of mechanical digestion in colon
- Haustral churning: distension reaches certain point and walls of haustra contract to squeeze contents onward and together to form/pack feces
- Peristalsis: localized propulsive contractions to move chyme
- Mass peristalsis: strong peristaltic wave that begins in transverse colon and quickly drives contents of colon to rectum
Major hormones of Digestive System
- gastrin
- secretin
- cholecystokinin
- leptin
Gastrin
- promotes secretion of gastric juice, increases gastric motility, relaxes pyloric sphincter
- Secreted b/c of stomach distention, when digested proteins are in stomach, and high pH of stomach chyme
Secretin
- stimulates secretion of pancreatic juice, inhibits secretion of gastric juice
- Secreted by S-cells in duodenum b/c of acidic chyme that enters SI
Cholecystokinin (CCK)
- inhibits gastric emptying
- stimulates secretion of bile
- induces satiety
- Secreted when chyme comes in SI
Leptin
- regulation of fat storage and acts on hypothalamus to decrease appetite
- Secreted when body has insulin secretion in body that lowers glucose levels
Peptic ulcers
- erosions of mucosa of alimentary canal in GI tract
- May occur in stomach or intestinal tract
- Caused by H. pylori bacteria over secreting acid that mucus can’t protect tissues
Inflammatory bowel disease
- inflammation of intestinal wall
- Caused by improper diet, microbiome disruption, damage to intestinal wall
- 2 disorders: Crohn’s disease and Ulcerative colitis
Cirrhosis
- when liver blood vessels destroyed and replaced by fibrotic scar tissue
- Leads to improper removal of bilirubin, jaundice, mood swings
Caused by hepatitis virus, alcoholism, bad diet
Cholelithiasis / Gallstones
- mineral deposits containing cholesterol that blocks bile ducts
- Causes pain, nausea, fever, vomiting, dark urine, pale stools
GERD
- stomach contents flows up to esophagus b/c esophageal sphincter didn’t close ⇒ acid flowed back up
- Treated with antacids or proton pump inhibitors (stops hydrogen ion release b/c protons are the ones causing acidity)
- Causes heartburn, dental issues, esophagitis, dysphagia
