DIGESTION, ABSORPTION AND RENAL SYSTEM Flashcards
WHAT TYPE OF GLYCOSIDIC BONDS ALLOWS FOR BRANCHING OF GLUCOSE RESIDUES (E.G. IN THE POLYSACCHARIDE STARCH)
ALPHA 1,6 GLYCOSIDIC BONDS
MECHANICAL AND CHEMICAL DIGESTION OF CARBOHYDRATES BEGINS WHERE?
in the mouth
WHAT ENZYME BREAKS DOWN THE ALPHA 1,4 GLYCOSIDIC BONDS?
ALPHA-AMYLASE
WHAT IS THE NAME OF THE LINEAR AND WHAT OF THE BRANCHED COMPONENT OF STARCH?
AMYLOSE - LINEAR
AMYLOPECTIN - BRANCHED
WHERE DOES THE MOST AND WHERE DOES THE LEAST OF CARBOHYDRATE DIGESTION OCCUR?
MOST IN THE SMALL INTESTINE, LEAST IN THE STOMACH
WHAT ARE AMYLOSE AND AMYLOPECTIN BROKEN DOWN INTO BY THE SALIVARY AMYLASE?
SMALLER CHAINS OF GLUCOSE CALLED DEXTRINS AND THE DISACCHARIDE MALTOSE
WHERE IS ALPHA AMYLASE DENTAURED?
IN THE STOMACH
THE MOST IMPORTANT ENZYME IN THE CARBOHYDRATE DIGESTION?
PANCREATIC AMYLASE
HOW ARE DISACCHARIDES BROKEN DOWN INTO MONOSACCHARIDES IN THE SMALL INTESTINE?
BY DISACCHARIDASES IN THE LUMINAL MEMBRANE OF THE BRUSH BORDER
WHAT DOES THE PANCREATIC ALPHA AMYLASE DO AFTER IT IS RELEASED INTO THE SMALL INTESTINE AS A COMPONENT OF PANCREATIC JUICE?
RESUMES THE BREAKDOWN OF DEXTRINS INTO SHORTER CARB CHAINS, MALTOSE AND OTHER DISACCHARIDES
ONCE CARBOHYDRATES ARE BROKEN DOWN INTO MONOSACCHARIDES (GLUCOSE, FRUCTOSE OR GALACTOSE), HOW AND WHERE ARE THEY TRANSPORTED?
INTO THE INTESTINAL CELLS, GLUCOSE AND GALACTOSE VIA ACTIVE TRANSPORT, FRUCTOSE VIA FACILITATED DIFFUSION
CHAIN OF UP TO HOW MANY AMINO ACIDS CAN BE SAFELY ABSORBED BY HUMANS?
UP TO 3 (TRIPEPTIDES)
WHERE DOES CHEMICAL (ENZYMATIC) DIGESTION (BREAKING DOWN OF PEPTIDE BONDS) OF THE PROTEINS START?
IN THE STOMACH
WHAT KIND OF PROTEIN DIGESTION OCCURS IN THE MOUTH?
MECHANICAL; LARGE PROTEIN PIECES SEPARATED THROUGH CHEWING
HOW ARE PROTEINS DENATURED AND THEIR 3D STRUCTURE UNFOLDED?
BY THE HYDROCHLORIC ACID
WHAT TYPES OF PROTEIN DIGESTION OCCUR IN THE STOMACH?
CHEMICAL AND MECHANICAL
WHICH CELLS SECRETE HCl?
PARIETAL
WHICH CELLS SECRETE PROENZYME (ZYMOGEN) PEPSINOGEN?
CHIEF (AKA ZYMOGENIC CELLS)
WHAT IS PEPSINOGEN?
INACTIVE FORM OF ENZYME PEPSIN RELEASED BY THE CHIEF CELLS IN THE STOMACH
WHAT STIMULATES CONVERSION OF PEPSINOGEN TO PEPSIN?
HCl LOWERING THE pH TO 3.5 (OPTIMAL pH FOR PEPSIN!!!)
WHAT PERCENTAGE OF INGESTED PROTEINS ARE DIGESTED BY PEPSIN AND WHAT DOES PEPSIN DO EXACTLY?
20%, BREAKS PEPTIDE BONDS
ORDER THE MAIN NUTRIENTS BASED ON THE TIME REQUIRED FOR THEIR DIGESTION, FROM LONGEST TO SHORTEST?
FAT, PROTEIN, CARBOHYDRATES
WHAT DOES DENATURATION DO TO PROTEINS?
MAKES THEM LOSE THEIR FUNCTION?
WHY IS INSULIN INJECTED RATHER THAN INGESTED?
BECAUSE IT IS A PROTEIN AND ITS FUNCTION WOULD BE DESTROYED BY DENATURATION AND ENZYMATIC FUNCTION IN THE STOMACH
WHERE DOES THE MAJORITY OF PROTEIN DIGESTION OCCUR?
IN THE SMALL INSTESTINE
WHAT ARE THE TWO PHASES OF PROTEIN DIGESTION IN THE SMALL INTESTINE?
LUMINAL PHASE - IN THE LUMEN OF THE INTESTINE WHERE DIGESTIVE JUICES ARE SECRETED
BRUSH BORDER PHASE - BY ENTEROCYTES AND MICROVILLI
WHAT ARE THE TWO MAJOR PANCREATIC PROTEASES (ENZYMES FOR PROTEIN DIGESTION)?
TRYPSIN AND CHYMOTRYPSIN
IN WHICH FORM DO THE PANCREATIC PROTEASES LEAVE THE PANCREAS?
PACKAGED INTO SECRETORY VESICLES AS INACTIVE PROENZYMES CALLED TRYPSINOGEN AND CHYMOTRYPSINOGEN
WHY ARE PANCREATIC PROTEASES RELEASED IN VESICLES, IN PRECURSOR FORM AND INCLUDING TRYPSIN INHIBITOR?
BECAUSE THEY ARE POTENTIALLY DANGEROUS ENZYMES IF ACTIVATED AT A WRONG PLACE
HOW ARE THE PANCREATIC PROTEASES ACTIVATED?
TRYPSINOGEN IS ACTIVATED (CONVERTED TO TRYPSIN) BY THE ENZYME ENTEROKINASE. TRYPSIN THEN ACTIVATES CHYMOTRIPSINOGEN AND ANY REMAINING MOLECULES OF TRYPSINOGEN.
CLASSIFICATION OF PROTEASES AND THE DIFFERENCE?
ENDOPEPTIDASES: CLEAVE PROTEINS IN THE MIDDLE OF THEIR CHAINS (TRYPSIN AND CHYMOTRYPSIN)
EXOPEPTIDASES: CLEAVE SINGLE AMINO ACIDS OFF THE FREE CARBOXYL ENDS OF PROTEINS
WHERE IS ENTEROKINASE RELEASED FROM?
DUODENAL MUCOSA
TRIPEPTIDES, DIPEPTIDES AND SINGLE AMINO ACIDS ENTER THE ENTEROCYTES BY ACTIVE OR PASSIVE TRANSPORT?
ACTIVE; REQUIRES ATP
WHAT HAPPENS TO THE PROTEINS WHICH AREN’T FULLY DIGESTED IN THE INTESTINE?
THEY PASS INTO THE COLON AND ARE EXCRETED IN FECES
HOW MUCH GRAMS OF FAT DOES FECES CONTAIN PER DAY?
LESS THAN 5g
WHICH MAIN NUTRIENT IS NOT WATER SOLUBLE?
LIPIDS
WHAT HAPPENS TO LIPIDS IN A WATERY ENVIRONMENT (LIKE THE GI TRACT)
THEY CLUSTER TOGETHER IN DROPLETS
WHERE DOES THE MOST OF ENZYMATIC DIGESTION OF LIPIDS OCCUR?
SMALL INTESTINE
WHERE IS THE LINGUAL LIPASE PRODUCED AND WHAT DOES IT DO?
BY THE CELLS ON THE TOUNGE, BEGINS SOME OF THE ENZYMATIC TRIGLYCERIDE DIGESTION
WHARE ARE THE NAMES OF LIPASES ACTIVE IN THE STOMACH?
GASTRIC AND LINGUAL LIPASE
HOW ARE BILE SALTS ABLE TO EMULSIFY WATER AND FAT, AND WHERE ARE THEY RELEASED
THEY ARE RELEASED IN THE DUODENUM. THEY HAVE HYDROPHOBIC AND HYDROPHILIC SIDES SO THEY ATTRACT BOTH FAT AND WATER.
WHY ARE LIPIDS EMULSIFIED?
TO BREAK DOWN FAT GLOBULES INTO SMALLER DROPLETS AND MAKE THEM MORE EASILY ACCESSIBLE BY DIGESTIVE ENZYMES BY INCREASING THE SURFACE AREA ON WHICH THEY CAN ACT
WHAT ARE MICELLES?
SMALL DROPLETS OF FAT SURROUNDED BY BILE
DO FAT SOLUBLE-VITAMINS AND CHOLESTEROL REQUIRE ENZYMATIC DIGESTION?
NO
WHAT IS THE ROLE OF PANCREATIC LIPASE AND WHAT ARE THE PRODUCTS OF ITS FUNCTIONING?
BREAKDOWN OF TRIGLYCERIDES AFTER THEY’VE BEEN EMULSIFIED, PRODUCING FREE FATTY ACIDS, MONOGLYCERIDES AND GLYCEROL
FAT PERCENTAGE OF BREAST MILK?
4%
WHAT PERCENTAGE OF INFANT’S CALORIES COMES FROM FAT?
50%
HOW ARE INFANTS ADAPTED TO DIGEST FAT, SINCE THEIR BILE AND PANCREATIC LIPASE LEVELS ARE LOW?
ACTIVITY OF THEIR GASTRIC AND LINGUAL LIPASES IS INCREASED AND THEY RECEIVE INACTIVE LIPASES IN BREAST MILK, WHICH ARE ACTIVATED IN THE BABY’S SMALL INTESTINE
WHY IS DONATED BREAST MILK HARDER TO DIGESTED THAN THE MILK STRAIGHT FROM THE BREAST?
BECAUSE HEAT DENATURATES LIPASES
HOW MANY MICRO ORGANISMS EXIST IN THE HUMAN GI TRACT?
100 TRILLION
WHICH ORGAN OF THE GI TRACT CONTAINS THE MOST OF MICROORGANISMS?
THE COLON
WHY ARE DIETARY FIBERS (WHOLEGRAINS) LINKED TO LOWER RISKS OF CVD AND T2D?
BECAUSE THEY ARE DIGESTED MUCH LESS IN THE GI TRACT (CANNOT BE BROKEN DOWN INTO SINGLE SUGAR MOLECULES) SO THE RISE IN GLUCOSE LEVELS AFTER A FIBER RICH MEAL IS MUCH LOWER THAN FOR OTHER TYPES OF CARBS (E.G. SIMPLE SUGARS, MANY STARCHES)
WHAT IS THE MAIN SOURCE OF ENERGY FOR COLONOCYTES?
SHORT CHAIN FATTY ACIDS (LESS THAN 6 CARBONS)
DO DIGESTION AND ABSORPTION OCCUR AT THE SAME TIME IN THE SMALL INTESTINE?
YES
HOW IS WATER ABSORBED ACROSS THE MUCOSA?
VIA OSMOSIS
WHICH CO.TRANSPORTER IS USED TO GET GLUCOSE INTO CELLS AND WHICH IONS ARE COTRANSPORTED WITH IT?
SGLT1, Na+
WHICH GLUCOSE TRANSPORTER MOVES GLUCOSE FROM THE CELL INTO THE PORTAL CIRCULATION, GOING TO THE LIVER?
GLUT2
HOW DOES Na+ THAT ENTERS ENTEROCYTES WITH GLUCOSE LEAVE THE CELLS?
IT IS ACTIVELY PUMPED OUT AND INTO THE INTERSTITIAL FLUID BY Na+/K+ ATPase
HOW DOES DIET HIGH IN CARBS INFLUENCE SGLT1 AND GLUT2 EXPRESSION LEVELS IN ENTEROCYTES?
IT INCREASES THEM
HOW ARE THE SHORT AND MEDIUM FREE FATTY ACIDS ABSORBED?
ONCE THEY ENTER THE ENTEROCYTES, THEY CAN FREELY BE ABSORBED INTO THE BLOOD VIA CAPILLARY
WHAT HAPPENS TO LONG CHAIN FREE FATTY ACIDS (MORE THAN 12C) IN ENTEROCYTES?
THEY ARE RE-ASSOCIATED WITH GLYCEROL BACKBONE AND TRIGLYCERIDES ARE FORMED AGAIN
WHAT DO TRIGLYCERIDES FORM IN ENTEROCYTES AND HOW?
THEY ARE JOINED BY A PROTEIN CARRIER, CHOLESTEROL ESTERS AND PHOSPHOLIPIDS TO FORM CHYLOMICRONS
WHAT KIND OF DIET FACILITATES AND WHAT KIND DECREASES CHOLESTEROL ABSORPTION?
DIET HIGH IN FAT HELPS CHOLSTEROL ABSORPTION, AND DIET HIGH IN FIBER (VEG, FRUIT, OATS) PREVENT CHOLESTEROL ABSORPTION BY BINDING BILE SALTS INSTEAD OF IT
HOW LONG DO CHYLOMICRONS CIRCULATE THROUGH THE BODY BEFORE RELEASING THEIR TRIGLYCERIDES?
10 HRS
WHAT HAPPENS TO REMNANTS OF CHYLOMICRONS AFTER THEY RELEASE TRIGLYCERIDES?
LIVER USES THEM TO FORMULATE SPECIFIC LIPOPROTEINS
TYPES AND FUNCTIONS OF LIPOPROTEINS?
VLDLS (VERY LOW DENSITY LIPOPROTEINS): transport triglycerides from the liver to bodily tissues
LDLs (LOW DENSITY LIPOPROTEINS): made out of more than 50% of cholesterol, carry cholesterol around the body
HDLs (HIGH DENSITY LIPOPROTEINS): carry cholesterol out of the blood stream and into the liver, mostly made out of protein, only 20-30% cholesterol
WHAT ARE THE CAUSES AND RESULTS OF LDL RECEPTOR INHIBITION?
CAUSE: DIET RICH IN SATURATED FATS
RESULT: HIGH LEVELS OF CHOLESTEROL REMAIN IN THE BLOODSTREAM AND CAN CAUSE HEART DISEASE OR ATHEROSCLEROSIS
HOW ARE AMINO ACIDS TRANSPORTED INTO EPITHELIAL CELLS, AND HOW INTO THE CAPILLARY BED?
1) BY SECONDARY ACTIVE TRANSPORT COUPLED TO Na+ TRANSPORT
2) VIA FACILITATED DIFFUSION
BREAKDOWN OF AMINO ACIDS IN THE LIVER WILL RESULT IN THE RELEASE OF? WHAT HAPPENS WITH THIS PRODUCT?
NITROGEN.CONTAINING AMMONIA RELEASED. IT IS TOXIC SO THE LIVER TRANSFORMS IT INTO UREA WHICH IS TRANSPORTED INTO KIDNEYS AND EXCRETED IN URINE
SYMPTOMS OF KIDNEY FAILURE?
HIGH BP, EXTREME TIREDNESS OR LETHARGY, PERSISTENT HEADACHES, SWELLING IN FACE AND ANKLES, FLUID RETENTION AND LOWER BACK PAIN
WHAT ARE THE MOST COMMON WASTE PRODUCTS THAT REACH THE KIDNEYS?
UREA AND CREATININE
WHAT PERCENTAGE OF INGESTED FLUID IS EXCRETED WITHIN AN HOUR?
CCA 80%
KIDNEY FUNCTIONS:
- FILTERS FOR GETTING RID OF BODY WASTE AND TOXIC SUBSTANCES
- RETURN VITAL SUBSTANCES (LIKE VITAMINS, AMINO ACIDS, GLUCOSE AND HORMONES) BACK INTO THE BLOOD STREAM
- MAINTAIN CORRECT BALANCE OF WATER AND ELECTROLYTES
- HORMONE SECRETION
WHAT IS RENIN?
A HORMONE SECRETED BY THE KIDNEYS WHICH HELPS MAINTAIN THE BP NORMAL BY CONSTRICTING THE SMALL BLOOD VESSELS THEREBY INCREASING BP
KIDNEY COLOUR, SHAPE, LENGTH, WIDTH, WEIGHT?
DARK RED, BEAN SHAPED, 10-15CM, 6CM, 150g
WHAT PERCENTAGE OF BODY WEIGHT DO KIDNEYS MAKE UP?
0.5%
WHAT PERCENTAGE OF CARDIAC OUTPUT IS RECEIVED BY THE KIDNEYS?
20%
WHERE ARE THE KIDNEYS LOCATED AND WHICH GLANDS ARE THEY IN CONTACT WITH?
HIGH IN THE ABDOMINAL CAVITY
ADRENAL GLANDS
HOW DOES BLOOD GET IN AND OUT OF THE KIDNEYS?
IN: RENAL ARTERIES WHICH ARISE FROM THE ABDOMINAL AORTA
OUT: LARGE VEINS JOINING INFERIOR VENA CAVA
WHAT IS THE NAME OF THE INNER AND WHAT IS THE NAME OF THE OUTER REGION OF THE KIDNEY?
INNER: THE MEDULLA
OUTER: RENAL CORTEX
KIDNEYS ARE DIVIDED INTO HOW MANY LOBES?
6-8
WHAT ARE THE 2 CHARACTERISTIC FEATURES OF THE KIDNEY MEDULLA?
RENAL PYRAMIDS AND RENAL PAPILLAE
HOW MANY NEPHRONS ARE THERE IN EACH KIDNEY?
1.3 MILLION
WHAT ARE NEPROHNS AND WHAT IS THEIR FUNCTION?
FUNCTIONAL UNITS OF THE KIDNEY THAT FILTER THE BLOOD AND BALANCE THE CONSTITUENTS OF CIRCULATION
WHAT ARE THE GLOMERULUS AND WHAT IS THE FUNCTION?
A PART OF THE NEPHRON, A SYSTEM OF HIGH PRESSURE CAPILLARIES THAT FILTER THE BLOOD BASED ON PARTICLE SIZE AND RECOVER MOST OF THE SOLUTES AND THE WATER, RETURNING THEM TO CIRCULATION.
HOW MUCH FLUID IS FILTERED BY THE KIDNEYS DAILY AND HOW MUCH IS EXCRETED?
180L, 1.5L
WHERE DOES THE MOST OF THE NaCl REABSORPTION OCCUR IN THE KIDNEY?
THE LOOP OF HENLE
WHAT IS GLYCOSURIA?
GLUCOSE DETECTED IN THE URINE, RARE
DESCRIBE GLUCOSE REABSORPTION FROM THE KIDNEY?
UPTAKE FROM THE LUMEN BY THE Na+ glucose co-transporter (SGLT1, but SGLT2), along the Na+ gradient created by Na+-K+-ATPase
PASSAGE FROM THE CELLS INTO THE BLOOD BY GLUT2
MOST GLUCOSE IS REABSORBED FROM THE KIDNEY VIA WHICH TRANSPORTER?
SGLT2 (90%)
NORMAL BLOOD GLUCOSE CONCENTRATIONS?
3.9-5.5 mmol/L
GLUT2 TRANSPORTER WILL GET SATURATED AND GLUCOSE WILL APPEAR TO URINE IF THE BLOOD LEVELS ARE:
10 mmol/L
GLIFLOZINS ARE?
A GROUP OF DRUGS THAT SPECIFICALLY BLOCKS SGLT2 SO THAT GLUCOSE IS NOT REABSORBED (PROMISING FOR T2D MANAGEMENT)
WHAT PERCENTAGE OF AMINOACIDS IS REABSORBED FROM THE KIDNEYS?
98%
WHAT ARE THE ENDOCRINE FUNCTIONS OF THE KIDNEYS?
- REGULATE THE PRODUCTION OF ERYTHROPOIETIN (PROTECTS THE RED BLOOD CELLS FROM DESTRUCTION, STIMULATES RED BLOOD CELL PRODUCTION FROM ERYTHROCYTES)
- VITAMIN D METABOLISM
- RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS)
- CONTROLS THE DEGRADATION OF A NUMBER OF PEPTIDE HORMONES
WHAT IS THE ROLE OF RAAS?
IT IS IMPORTANT FOR HANDLING OF SODIUM AND WATER BY THE KIDNEYS (BECAUSE Na+ AND WATER WILL CHANGE THE VOLUME OF FLUID IN THE BODY, RAAS PLAYS A GREAT ROLE IN REGULATING BLOOD VOLUME)
WHAT KIDNEY CELLS SIT SIDE BY SIDE AND DETECT AND RESPOND TO CHANGES IN NaCl?
THE MACULA DENSA CELLS: DETECT NaCl CHANGES AND CHANGES IN THE PRESSURE IN THE TUBULAR FLUID
THE ADJACENT JUXTAGLOMERULAR (JG) CELLS: SECRETE RENIN IN RESPONSE TO SIGNALS SENT BY THE MACULA DENSA
WHICH CELLS SECRETE RENIN?
JUXTAGLOMERULAR (JG) CELLS
WHAT DO MACULA DENSA CELLS RELEASE WHEN THE PRESSURE AND NaCl CONCENTRATION ARE REDUCED TO STIMULATE RENIN PRODUCTION?
PROSTAGLANDINE E2 (PGE2)
WHERE IS THE PEPTIDE ANGIOTENSINOGEN SYNTHESIZED?
THE LIVER
WHAT IS ANGIOTENSINOGEN CONVERTED INTO AND BY WHICH ENZYME?
RENIN CONVERTS IT INTO ANGIOTENSIN I
WHAT IS ANGIOTENSIN I CONVERTED INTO AND BY WHICH HORMONE?
IT IS CONVERTED INTO ANGIOTENSIN II BY ANGIOTENSIN CONVERTING HORMONE (ACE)
ANGIOTENSIN II ACTS ON ANGIOTENSIN RECEPTORS LOCATED IN SEVERAL TARGET TISSUES, FOR EXAMPLE:
ADRENAL GLANDS, KIDNEYS, BRAIN AND VASCULATURE…
ANGIOTENSIN II IS A POTENT:
VASOCONSTRICTOR!!!!!!, SLOWS DOWN THE BLOOD FLOW THAT IS FILTERED BY THE GLOMERULUS
WHAT HAPPENS WHEN ANGIOTENSIN RECEPTORS ON ADRENAL CORTEX ARE STIMULATED?
ALDOSTERONE IS RELEASED FROM ADRENAL GLANDS
WHAT DOES ALDOSTERONE DO?
INCREASES SODIUM AND WATER REABSORPTION BY THE KIDNEY
ANGIOTENSIN II INCREASES OR DECREASES SODIUM AND WATER REABSORPTION?
INCREASES
WHAT ARE THE EFFECTS OF ANGIOTENSIN II IN THE BRAIN?
STIMULATES THE SECRETION OF THE ANTI-DIURETIC HORMONE (ADH) FROM THE POSTERIOR PITUITARY WHICH FURTHER INCREASES WATER REABSORPTION AND BLOOD VOLUME AND STIMULATES THIRST!!
+ STIMULATES VASOPRESSIN SECRETION FROM THE POSTERIOR PITUITARY; VASOPRESSIN IS A VASOCONSTRICTOR
