DIGESTION, ABSORPTION AND RENAL SYSTEM Flashcards

1
Q

WHAT TYPE OF GLYCOSIDIC BONDS ALLOWS FOR BRANCHING OF GLUCOSE RESIDUES (E.G. IN THE POLYSACCHARIDE STARCH)

A

ALPHA 1,6 GLYCOSIDIC BONDS

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2
Q

MECHANICAL AND CHEMICAL DIGESTION OF CARBOHYDRATES BEGINS WHERE?

A

in the mouth

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3
Q

WHAT ENZYME BREAKS DOWN THE ALPHA 1,4 GLYCOSIDIC BONDS?

A

ALPHA-AMYLASE

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4
Q

WHAT IS THE NAME OF THE LINEAR AND WHAT OF THE BRANCHED COMPONENT OF STARCH?

A

AMYLOSE - LINEAR

AMYLOPECTIN - BRANCHED

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5
Q

WHERE DOES THE MOST AND WHERE DOES THE LEAST OF CARBOHYDRATE DIGESTION OCCUR?

A

MOST IN THE SMALL INTESTINE, LEAST IN THE STOMACH

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6
Q

WHAT ARE AMYLOSE AND AMYLOPECTIN BROKEN DOWN INTO BY THE SALIVARY AMYLASE?

A

SMALLER CHAINS OF GLUCOSE CALLED DEXTRINS AND THE DISACCHARIDE MALTOSE

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7
Q

WHERE IS ALPHA AMYLASE DENTAURED?

A

IN THE STOMACH

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8
Q

THE MOST IMPORTANT ENZYME IN THE CARBOHYDRATE DIGESTION?

A

PANCREATIC AMYLASE

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9
Q

HOW ARE DISACCHARIDES BROKEN DOWN INTO MONOSACCHARIDES IN THE SMALL INTESTINE?

A

BY DISACCHARIDASES IN THE LUMINAL MEMBRANE OF THE BRUSH BORDER

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10
Q

WHAT DOES THE PANCREATIC ALPHA AMYLASE DO AFTER IT IS RELEASED INTO THE SMALL INTESTINE AS A COMPONENT OF PANCREATIC JUICE?

A

RESUMES THE BREAKDOWN OF DEXTRINS INTO SHORTER CARB CHAINS, MALTOSE AND OTHER DISACCHARIDES

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11
Q

ONCE CARBOHYDRATES ARE BROKEN DOWN INTO MONOSACCHARIDES (GLUCOSE, FRUCTOSE OR GALACTOSE), HOW AND WHERE ARE THEY TRANSPORTED?

A

INTO THE INTESTINAL CELLS, GLUCOSE AND GALACTOSE VIA ACTIVE TRANSPORT, FRUCTOSE VIA FACILITATED DIFFUSION

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12
Q

CHAIN OF UP TO HOW MANY AMINO ACIDS CAN BE SAFELY ABSORBED BY HUMANS?

A

UP TO 3 (TRIPEPTIDES)

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13
Q

WHERE DOES CHEMICAL (ENZYMATIC) DIGESTION (BREAKING DOWN OF PEPTIDE BONDS) OF THE PROTEINS START?

A

IN THE STOMACH

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14
Q

WHAT KIND OF PROTEIN DIGESTION OCCURS IN THE MOUTH?

A

MECHANICAL; LARGE PROTEIN PIECES SEPARATED THROUGH CHEWING

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15
Q

HOW ARE PROTEINS DENATURED AND THEIR 3D STRUCTURE UNFOLDED?

A

BY THE HYDROCHLORIC ACID

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16
Q

WHAT TYPES OF PROTEIN DIGESTION OCCUR IN THE STOMACH?

A

CHEMICAL AND MECHANICAL

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17
Q

WHICH CELLS SECRETE HCl?

A

PARIETAL

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18
Q

WHICH CELLS SECRETE PROENZYME (ZYMOGEN) PEPSINOGEN?

A

CHIEF (AKA ZYMOGENIC CELLS)

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19
Q

WHAT IS PEPSINOGEN?

A

INACTIVE FORM OF ENZYME PEPSIN RELEASED BY THE CHIEF CELLS IN THE STOMACH

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20
Q

WHAT STIMULATES CONVERSION OF PEPSINOGEN TO PEPSIN?

A

HCl LOWERING THE pH TO 3.5 (OPTIMAL pH FOR PEPSIN!!!)

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21
Q

WHAT PERCENTAGE OF INGESTED PROTEINS ARE DIGESTED BY PEPSIN AND WHAT DOES PEPSIN DO EXACTLY?

A

20%, BREAKS PEPTIDE BONDS

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22
Q

ORDER THE MAIN NUTRIENTS BASED ON THE TIME REQUIRED FOR THEIR DIGESTION, FROM LONGEST TO SHORTEST?

A

FAT, PROTEIN, CARBOHYDRATES

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23
Q

WHAT DOES DENATURATION DO TO PROTEINS?

A

MAKES THEM LOSE THEIR FUNCTION?

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24
Q

WHY IS INSULIN INJECTED RATHER THAN INGESTED?

A

BECAUSE IT IS A PROTEIN AND ITS FUNCTION WOULD BE DESTROYED BY DENATURATION AND ENZYMATIC FUNCTION IN THE STOMACH

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25
Q

WHERE DOES THE MAJORITY OF PROTEIN DIGESTION OCCUR?

A

IN THE SMALL INSTESTINE

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26
Q

WHAT ARE THE TWO PHASES OF PROTEIN DIGESTION IN THE SMALL INTESTINE?

A

LUMINAL PHASE - IN THE LUMEN OF THE INTESTINE WHERE DIGESTIVE JUICES ARE SECRETED
BRUSH BORDER PHASE - BY ENTEROCYTES AND MICROVILLI

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27
Q

WHAT ARE THE TWO MAJOR PANCREATIC PROTEASES (ENZYMES FOR PROTEIN DIGESTION)?

A

TRYPSIN AND CHYMOTRYPSIN

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28
Q

IN WHICH FORM DO THE PANCREATIC PROTEASES LEAVE THE PANCREAS?

A

PACKAGED INTO SECRETORY VESICLES AS INACTIVE PROENZYMES CALLED TRYPSINOGEN AND CHYMOTRYPSINOGEN

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29
Q

WHY ARE PANCREATIC PROTEASES RELEASED IN VESICLES, IN PRECURSOR FORM AND INCLUDING TRYPSIN INHIBITOR?

A

BECAUSE THEY ARE POTENTIALLY DANGEROUS ENZYMES IF ACTIVATED AT A WRONG PLACE

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30
Q

HOW ARE THE PANCREATIC PROTEASES ACTIVATED?

A

TRYPSINOGEN IS ACTIVATED (CONVERTED TO TRYPSIN) BY THE ENZYME ENTEROKINASE. TRYPSIN THEN ACTIVATES CHYMOTRIPSINOGEN AND ANY REMAINING MOLECULES OF TRYPSINOGEN.

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31
Q

CLASSIFICATION OF PROTEASES AND THE DIFFERENCE?

A

ENDOPEPTIDASES: CLEAVE PROTEINS IN THE MIDDLE OF THEIR CHAINS (TRYPSIN AND CHYMOTRYPSIN)
EXOPEPTIDASES: CLEAVE SINGLE AMINO ACIDS OFF THE FREE CARBOXYL ENDS OF PROTEINS

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32
Q

WHERE IS ENTEROKINASE RELEASED FROM?

A

DUODENAL MUCOSA

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33
Q

TRIPEPTIDES, DIPEPTIDES AND SINGLE AMINO ACIDS ENTER THE ENTEROCYTES BY ACTIVE OR PASSIVE TRANSPORT?

A

ACTIVE; REQUIRES ATP

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34
Q

WHAT HAPPENS TO THE PROTEINS WHICH AREN’T FULLY DIGESTED IN THE INTESTINE?

A

THEY PASS INTO THE COLON AND ARE EXCRETED IN FECES

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35
Q

HOW MUCH GRAMS OF FAT DOES FECES CONTAIN PER DAY?

A

LESS THAN 5g

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36
Q

WHICH MAIN NUTRIENT IS NOT WATER SOLUBLE?

A

LIPIDS

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37
Q

WHAT HAPPENS TO LIPIDS IN A WATERY ENVIRONMENT (LIKE THE GI TRACT)

A

THEY CLUSTER TOGETHER IN DROPLETS

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38
Q

WHERE DOES THE MOST OF ENZYMATIC DIGESTION OF LIPIDS OCCUR?

A

SMALL INTESTINE

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39
Q

WHERE IS THE LINGUAL LIPASE PRODUCED AND WHAT DOES IT DO?

A

BY THE CELLS ON THE TOUNGE, BEGINS SOME OF THE ENZYMATIC TRIGLYCERIDE DIGESTION

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40
Q

WHARE ARE THE NAMES OF LIPASES ACTIVE IN THE STOMACH?

A

GASTRIC AND LINGUAL LIPASE

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41
Q

HOW ARE BILE SALTS ABLE TO EMULSIFY WATER AND FAT, AND WHERE ARE THEY RELEASED

A

THEY ARE RELEASED IN THE DUODENUM. THEY HAVE HYDROPHOBIC AND HYDROPHILIC SIDES SO THEY ATTRACT BOTH FAT AND WATER.

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42
Q

WHY ARE LIPIDS EMULSIFIED?

A

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

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43
Q

WHAT ARE MICELLES?

A

SMALL DROPLETS OF FAT SURROUNDED BY BILE

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44
Q

DO FAT SOLUBLE-VITAMINS AND CHOLESTEROL REQUIRE ENZYMATIC DIGESTION?

A

NO

45
Q

WHAT IS THE ROLE OF PANCREATIC LIPASE AND WHAT ARE THE PRODUCTS OF ITS FUNCTIONING?

A

BREAKDOWN OF TRIGLYCERIDES AFTER THEY’VE BEEN EMULSIFIED, PRODUCING FREE FATTY ACIDS, MONOGLYCERIDES AND GLYCEROL

46
Q

FAT PERCENTAGE OF BREAST MILK?

A

4%

47
Q

WHAT PERCENTAGE OF INFANT’S CALORIES COMES FROM FAT?

A

50%

48
Q

HOW ARE INFANTS ADAPTED TO DIGEST FAT, SINCE THEIR BILE AND PANCREATIC LIPASE LEVELS ARE LOW?

A

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

49
Q

WHY IS DONATED BREAST MILK HARDER TO DIGESTED THAN THE MILK STRAIGHT FROM THE BREAST?

A

BECAUSE HEAT DENATURATES LIPASES

50
Q

HOW MANY MICRO ORGANISMS EXIST IN THE HUMAN GI TRACT?

A

100 TRILLION

51
Q

WHICH ORGAN OF THE GI TRACT CONTAINS THE MOST OF MICROORGANISMS?

A

THE COLON

52
Q

WHY ARE DIETARY FIBERS (WHOLEGRAINS) LINKED TO LOWER RISKS OF CVD AND T2D?

A

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)

53
Q

WHAT IS THE MAIN SOURCE OF ENERGY FOR COLONOCYTES?

A

SHORT CHAIN FATTY ACIDS (LESS THAN 6 CARBONS)

54
Q

DO DIGESTION AND ABSORPTION OCCUR AT THE SAME TIME IN THE SMALL INTESTINE?

A

YES

55
Q

HOW IS WATER ABSORBED ACROSS THE MUCOSA?

A

VIA OSMOSIS

56
Q

WHICH CO.TRANSPORTER IS USED TO GET GLUCOSE INTO CELLS AND WHICH IONS ARE COTRANSPORTED WITH IT?

A

SGLT1, Na+

57
Q

WHICH GLUCOSE TRANSPORTER MOVES GLUCOSE FROM THE CELL INTO THE PORTAL CIRCULATION, GOING TO THE LIVER?

A

GLUT2

58
Q

HOW DOES Na+ THAT ENTERS ENTEROCYTES WITH GLUCOSE LEAVE THE CELLS?

A

IT IS ACTIVELY PUMPED OUT AND INTO THE INTERSTITIAL FLUID BY Na+/K+ ATPase

59
Q

HOW DOES DIET HIGH IN CARBS INFLUENCE SGLT1 AND GLUT2 EXPRESSION LEVELS IN ENTEROCYTES?

A

IT INCREASES THEM

60
Q

HOW ARE THE SHORT AND MEDIUM FREE FATTY ACIDS ABSORBED?

A

ONCE THEY ENTER THE ENTEROCYTES, THEY CAN FREELY BE ABSORBED INTO THE BLOOD VIA CAPILLARY

61
Q

WHAT HAPPENS TO LONG CHAIN FREE FATTY ACIDS (MORE THAN 12C) IN ENTEROCYTES?

A

THEY ARE RE-ASSOCIATED WITH GLYCEROL BACKBONE AND TRIGLYCERIDES ARE FORMED AGAIN

62
Q

WHAT DO TRIGLYCERIDES FORM IN ENTEROCYTES AND HOW?

A

THEY ARE JOINED BY A PROTEIN CARRIER, CHOLESTEROL ESTERS AND PHOSPHOLIPIDS TO FORM CHYLOMICRONS

63
Q

WHAT KIND OF DIET FACILITATES AND WHAT KIND DECREASES CHOLESTEROL ABSORPTION?

A

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

64
Q

HOW LONG DO CHYLOMICRONS CIRCULATE THROUGH THE BODY BEFORE RELEASING THEIR TRIGLYCERIDES?

A

10 HRS

65
Q

WHAT HAPPENS TO REMNANTS OF CHYLOMICRONS AFTER THEY RELEASE TRIGLYCERIDES?

A

LIVER USES THEM TO FORMULATE SPECIFIC LIPOPROTEINS

66
Q

TYPES AND FUNCTIONS OF LIPOPROTEINS?

A

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

67
Q

WHAT ARE THE CAUSES AND RESULTS OF LDL RECEPTOR INHIBITION?

A

CAUSE: DIET RICH IN SATURATED FATS
RESULT: HIGH LEVELS OF CHOLESTEROL REMAIN IN THE BLOODSTREAM AND CAN CAUSE HEART DISEASE OR ATHEROSCLEROSIS

68
Q

HOW ARE AMINO ACIDS TRANSPORTED INTO EPITHELIAL CELLS, AND HOW INTO THE CAPILLARY BED?

A

1) BY SECONDARY ACTIVE TRANSPORT COUPLED TO Na+ TRANSPORT

2) VIA FACILITATED DIFFUSION

69
Q

BREAKDOWN OF AMINO ACIDS IN THE LIVER WILL RESULT IN THE RELEASE OF? WHAT HAPPENS WITH THIS PRODUCT?

A

NITROGEN.CONTAINING AMMONIA RELEASED. IT IS TOXIC SO THE LIVER TRANSFORMS IT INTO UREA WHICH IS TRANSPORTED INTO KIDNEYS AND EXCRETED IN URINE

70
Q

SYMPTOMS OF KIDNEY FAILURE?

A

HIGH BP, EXTREME TIREDNESS OR LETHARGY, PERSISTENT HEADACHES, SWELLING IN FACE AND ANKLES, FLUID RETENTION AND LOWER BACK PAIN

71
Q

WHAT ARE THE MOST COMMON WASTE PRODUCTS THAT REACH THE KIDNEYS?

A

UREA AND CREATININE

72
Q

WHAT PERCENTAGE OF INGESTED FLUID IS EXCRETED WITHIN AN HOUR?

A

CCA 80%

73
Q

KIDNEY FUNCTIONS:

A
  • 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
74
Q

WHAT IS RENIN?

A

A HORMONE SECRETED BY THE KIDNEYS WHICH HELPS MAINTAIN THE BP NORMAL BY CONSTRICTING THE SMALL BLOOD VESSELS THEREBY INCREASING BP

75
Q

KIDNEY COLOUR, SHAPE, LENGTH, WIDTH, WEIGHT?

A

DARK RED, BEAN SHAPED, 10-15CM, 6CM, 150g

76
Q

WHAT PERCENTAGE OF BODY WEIGHT DO KIDNEYS MAKE UP?

A

0.5%

77
Q

WHAT PERCENTAGE OF CARDIAC OUTPUT IS RECEIVED BY THE KIDNEYS?

A

20%

78
Q

WHERE ARE THE KIDNEYS LOCATED AND WHICH GLANDS ARE THEY IN CONTACT WITH?

A

HIGH IN THE ABDOMINAL CAVITY

ADRENAL GLANDS

79
Q

HOW DOES BLOOD GET IN AND OUT OF THE KIDNEYS?

A

IN: RENAL ARTERIES WHICH ARISE FROM THE ABDOMINAL AORTA
OUT: LARGE VEINS JOINING INFERIOR VENA CAVA

80
Q

WHAT IS THE NAME OF THE INNER AND WHAT IS THE NAME OF THE OUTER REGION OF THE KIDNEY?

A

INNER: THE MEDULLA
OUTER: RENAL CORTEX

81
Q

KIDNEYS ARE DIVIDED INTO HOW MANY LOBES?

A

6-8

82
Q

WHAT ARE THE 2 CHARACTERISTIC FEATURES OF THE KIDNEY MEDULLA?

A

RENAL PYRAMIDS AND RENAL PAPILLAE

83
Q

HOW MANY NEPHRONS ARE THERE IN EACH KIDNEY?

A

1.3 MILLION

84
Q

WHAT ARE NEPROHNS AND WHAT IS THEIR FUNCTION?

A

FUNCTIONAL UNITS OF THE KIDNEY THAT FILTER THE BLOOD AND BALANCE THE CONSTITUENTS OF CIRCULATION

85
Q

WHAT ARE THE GLOMERULUS AND WHAT IS THE FUNCTION?

A

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.

86
Q

HOW MUCH FLUID IS FILTERED BY THE KIDNEYS DAILY AND HOW MUCH IS EXCRETED?

A

180L, 1.5L

87
Q

WHERE DOES THE MOST OF THE NaCl REABSORPTION OCCUR IN THE KIDNEY?

A

THE LOOP OF HENLE

88
Q

WHAT IS GLYCOSURIA?

A

GLUCOSE DETECTED IN THE URINE, RARE

89
Q

DESCRIBE GLUCOSE REABSORPTION FROM THE KIDNEY?

A

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

90
Q

MOST GLUCOSE IS REABSORBED FROM THE KIDNEY VIA WHICH TRANSPORTER?

A

SGLT2 (90%)

91
Q

NORMAL BLOOD GLUCOSE CONCENTRATIONS?

A

3.9-5.5 mmol/L

92
Q

GLUT2 TRANSPORTER WILL GET SATURATED AND GLUCOSE WILL APPEAR TO URINE IF THE BLOOD LEVELS ARE:

A

10 mmol/L

93
Q

GLIFLOZINS ARE?

A

A GROUP OF DRUGS THAT SPECIFICALLY BLOCKS SGLT2 SO THAT GLUCOSE IS NOT REABSORBED (PROMISING FOR T2D MANAGEMENT)

94
Q

WHAT PERCENTAGE OF AMINOACIDS IS REABSORBED FROM THE KIDNEYS?

A

98%

95
Q

WHAT ARE THE ENDOCRINE FUNCTIONS OF THE KIDNEYS?

A
  • 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
96
Q

WHAT IS THE ROLE OF RAAS?

A

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)

97
Q

WHAT KIDNEY CELLS SIT SIDE BY SIDE AND DETECT AND RESPOND TO CHANGES IN NaCl?

A

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

98
Q

WHICH CELLS SECRETE RENIN?

A

JUXTAGLOMERULAR (JG) CELLS

99
Q

WHAT DO MACULA DENSA CELLS RELEASE WHEN THE PRESSURE AND NaCl CONCENTRATION ARE REDUCED TO STIMULATE RENIN PRODUCTION?

A

PROSTAGLANDINE E2 (PGE2)

100
Q

WHERE IS THE PEPTIDE ANGIOTENSINOGEN SYNTHESIZED?

A

THE LIVER

101
Q

WHAT IS ANGIOTENSINOGEN CONVERTED INTO AND BY WHICH ENZYME?

A

RENIN CONVERTS IT INTO ANGIOTENSIN I

102
Q

WHAT IS ANGIOTENSIN I CONVERTED INTO AND BY WHICH HORMONE?

A

IT IS CONVERTED INTO ANGIOTENSIN II BY ANGIOTENSIN CONVERTING HORMONE (ACE)

103
Q

ANGIOTENSIN II ACTS ON ANGIOTENSIN RECEPTORS LOCATED IN SEVERAL TARGET TISSUES, FOR EXAMPLE:

A

ADRENAL GLANDS, KIDNEYS, BRAIN AND VASCULATURE…

104
Q

ANGIOTENSIN II IS A POTENT:

A

VASOCONSTRICTOR!!!!!!, SLOWS DOWN THE BLOOD FLOW THAT IS FILTERED BY THE GLOMERULUS

105
Q

WHAT HAPPENS WHEN ANGIOTENSIN RECEPTORS ON ADRENAL CORTEX ARE STIMULATED?

A

ALDOSTERONE IS RELEASED FROM ADRENAL GLANDS

106
Q

WHAT DOES ALDOSTERONE DO?

A

INCREASES SODIUM AND WATER REABSORPTION BY THE KIDNEY

107
Q

ANGIOTENSIN II INCREASES OR DECREASES SODIUM AND WATER REABSORPTION?

A

INCREASES

108
Q

WHAT ARE THE EFFECTS OF ANGIOTENSIN II IN THE BRAIN?

A

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