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305 Cards in this Set
- Front
- Back
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State the two functions of bile.
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1. Excretion
2. Absorption (emulsification) of fats + fat-sol. vitamins |
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What are the primary bile acids and where are they produced?
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Cholic acid + Chenodeoxycholic acid
Hepatocytes (made from cholesterol) |
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How and where are primary bile acids conjugated to secondary bile salts?
Also, name them. |
Lithocholic acid and deoxycholic acid.
In the small intenstine, primary bile salts are conjugated with glycine and taurine to produce secondary bile salts. |
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What does the gall bladder do?
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Stores and concentrates bile.
Concentration: Removes salts and H2O from bile. Na+ ions are exchanged for H+ ions. Cl- ions are exchanged for HCO3- ions. (ALKALINE FLUID, REMEMBER?!) |
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What stimulates gall bladder emptying?
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CCK + Ach
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Two types of gallstones:
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Cholesterol (80%)
Pigment (20%) |
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Where are lipids absorbed?
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Small intestine, mostly duodenum.
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What are apolipoproteins?
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Structural protein compnents of lipoproteins.
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Name of the pathway that transports dietary fats to the blood?
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Exogenous pathway
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Which lipoprotein has the lowest density?
And which has the highest? |
Lowest: Chylomicron
Highest: HDL |
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Describe the structure of lipoproteins.
(as in, the core and the surface stuff) |
Tryglyceride non-polar core
Polarised Phospholipid mono-layer surface with cholesterol also, there are apolipoproteins for extra structure |
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ApoB (apolipoprotein B) is found in which lipoproteins?
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Chylomicrons
VLDL LDL |
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ApoE (apolipoprotein E) is found in which lipoprotein?
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IDL
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ApoC-II (apolipoprotein C-II) is found in which lipoprotein?
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Chylomicrons
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what are lacteals?
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lymphatic vessels in the villi of s. intestine.
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where are triglycerides packaged into chylomicrons?
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RER of enterocytes
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How do chylomicrons enter the blood?
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Exocytosis into lacteals.
--->through lymph system ----> through thoracic duct ---->BLOOD |
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What enzyme does ApoC-II activate on chylomicrons?
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Lipoprotein lipase
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Where does lymph drain to?
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(posterior mediastinum)
Thoracic duct ---> Left + right subclavian veins |
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Where does the lymph from the breast drain to?
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75% Axillary nodes
25% parasternal nodes |
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Islets of Langerhans.
Which cells secrete what? |
alpha = glucogon
beta = insulin delta = somatostatin |
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Which enzyme converts pyruvate ---> Actetyl CoA?
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PDH
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Which enzyme converts Acetyl CoA ---> Malonyl CoA?
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Acetyl-CoA Carboxylase
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Which enzyme converts Malonyl-CoA ---> Fatty Acid?
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Fatty Acid Synthase
(NADPH also required) |
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How much glycogen does the liver store?
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100g
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What happens when glucose can no longer be converted to glycogen in the liver?
(because there's already 100g glycogen) |
Glucose ---> Fatty acids
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What does insulin do to hormone sensitive lipase (HSL)?
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Inhibits it
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What hormone converts glucose to glucose-6-phosphate in the:
i. liver ii. muscle |
i. Glucokinase
ii. Hexokinase |
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How much water is absorbed in the DUODENUM per day?
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8-10L
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How much water is absorbed in the SMALL INTESTINE per day?
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6-10L
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How much water is absorbed in the COLON per day?
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4L
(2L ileocaecal + 2L colon) |
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Cause/mechanism of osmotic diarrhoea?
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Osmotic particles (eg. sorbital, Mg salts) are not absorbed by small intestine.
Increases osmolality of intestinal contents, reducing water absorption. |
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Mechanism of secretory diarrhoea?
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Ion transport defect. Inbalance between absorption/secretion.
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Lactase deficiency
Glucose-galactose malabsorption The above are examples of what kind of diarrhoea? |
Osmotic
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What is the effect of fasting on:
i. Osmotic diarrhoea? ii. Secretory? |
i. Diarrhoea stops
ii. Diarrhoea continues |
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What is an osmotic gap in diarrhoea?
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Faecal osmolality - Faecal electrolytes
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Osmotic or secretory diarrhoea: which has the larger osmotic gap?
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Osmotic. (High faecal osmolality + normal electrolyte levels)
(Secretory has high faecal osmolality + high faecal electrolyte levels) |
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Neuroendocrine Substances that increase gut motility?
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Ach,
Substance P, |
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Neuroendocrine Substances that decrease gut motility?
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NE
NO ATP VIP |
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Can polysaccharides be absorbed?
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Nope.
Must be converted to monosaccharides first. |
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Where are carbohydrates (monosaccharides) absorbed?
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Small intestine.
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Where can we find the cells that absorb monosaccharides?
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On the villi of the small intestine.
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Amylose is broken down into what?
Using what enzymes? |
Amylose ---> Maltotriose ---> Maltose ----> Glucose
Amylase Maltase |
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Which transporter takes up glucose and galactose into enterocytes?
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SGLT1
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Which transporter takes up fructose into enterocytes?
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GLUT5
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GLUT2 transporter: what does it do?
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Transports glucose, galactose and fructose from enterocytes into the blood.
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Which bonds does amylase break?
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alpha, 1-4 glycosidic (in amylose and amylopectin)
(cannot break down the branched 1,6 alpha bonds of amylopectin) |
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What is amylopectin?
And what enzymes breaks down amylopectin? |
Branched form of starch.
Amylopectin ---> Alpha-limit dextrins ----> glucose Amylase breaks the alpha 1,4 glycosidic bonds. Sucrase-isomaltase breaks down the alpha-limt dextrins into glucose. |
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Main type of food that contains lactose?
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Dairy.
MILK |
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Symptoms of lactose intolerance?
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Osmotic diarrhoea, cramps, flatulence
after consumption of lactose |
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Deficiency of either lactase, SGLT1 or sucrase-isomaltase...
What are the signs/symptoms? |
Osmotic diarrhoea, cramps, flatulence
Increased H2 in breath (due to bacterial fermentation) |
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In one sentence, what is the endogenous pathway?
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Transferring the lipids synthesised in the liver to the peripheral/adipose tissues.
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ENDOGENOUS PATHWAY:
What three substances does the liver package into VLDL lipoproteins? |
Triglycerides
Cholesterol ApoB |
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ENDOGENOUS PATHWAY:
What do nascent VLDL lipoproteins "steal" in order to mature? |
ApoC-11
and ApoE from HDL |
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ENDOGENOUS PATHWAY:
What does lipoprotein lipase (LPL) do to VLDL? |
Triglycerides ----> fatty acids + glycerol
FA + glycerol then released into adipose tissue |
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ENDOGENOUS PATHWAY:
How is VLDL converted to IDL? |
ApoC-II is returned to HDL.
HDL gives the IDL some cholesterol. |
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ENDOGENOUS PATHWAY:
IDL ---> LDL What enzyme catalyses this reaction? |
Hepatic Lipase
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ENDOGENOUS PATHWAY:
What receptors does LDL bind to in order to be taken up into the cell? |
LDLr
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ENDOGENOUS PATHWAY:
When LDL is released into the blood, what does it do? |
Binds to LDLr receptors on peripheral tissues
Taken up into these tissues Releases cholesterol into these tissues |
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REVERSE CHOLESTEROL TRANSPORT:
What even is it? |
Excess cholesterol is transported via HDL from peripheral tissues ---> liver.
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REVERSE CHOLESTEROL TRANSPORT:
Which receptor on peripheral tissue cells transports cholesterol out of the cells, to the HDL? |
ABCA1
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REVERSE CHOLESTEROL TRANSPORT:
Which receptor on the liver uptakes cholesterol from HDL into the liver? |
SR-B1
(scavenger receptor- class B) |
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CHOLESTEROL HOMEOSTASIS:
Name the rate-limiting enzyme in cholesterol synthesis. |
HMG-CoA reductase
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CHOLESTEROL HOMEOSTASIS:
Function and Mechanism of SREBP2? (sterol sensor protein) |
Triggered by high cholesterol lvls in liver.
Its function is to REDUCE CHOLESTEROL. 1. Inhibits HMG-CoA reductase (reduces synthesis of cholesterol) 2. Blocks LDLR (reduces intake of cholesterol from LDL lipoproteins in the blood) |
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What do statins inhibit, in order to lower cholesterol?
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HMG-CoA Reductase
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What do i. endopeptidases and ii. exopeptidases do?
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i. Endopeptidases break specific peptide bonds within a protein chain.
ii. Exopeptidases break off amino acids from the end of the chain, |
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Trypsin
Chymotrypsin Elastase --->endopeptidases or exopeptidases? Oh, and where are they found? And what do they DO? |
Endopeptidases.
Intestinal lumen Break down polypeptides into oligopeptides. |
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What peptide is present in the stomach?
And what does it do? |
PEPSIN
Proteins ----> Polypeptides |
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Carboxypeptidase A
Carboxypeptidase B What are these things? And what do they do? |
eXopeptidases of the intestinal lumen stage.
Break down polypeptides into oligopeptides. |
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Where are brush border peptidases found?
aaaaaaand...what do they do? |
small intestine brush border
Break down oligopeptides into di/tripeptides + amino acids |
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What converts di/tripeptides to amino acids?
AND WHERE? |
Cytosolic peptidases ...in the cytosol.
eg. Prolidase |
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What converts trypsinogen to trypsin?
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Enterokinase.
Found in the duodenal mucosa. |
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What symptoms does a trypsin deficiency cause?
And what about enterokinase deficiency? |
Hypoproteinaemia ---> reduced oncotic pressure
---> Oedema, severe diarrhoea, failure to thrive Enterokinase presents in the same way. |
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What is prolidase?
And what would a prolidase deficiency cause? |
Cytosolic exopeptidase
Impaired collagen turnover ---> skin lesions |
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3 sources of nitrogen (amino acids) in the body:
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1. Dietary protein
2. Breakdown of tissue proteins 3. de novo synthesis of non-essential amino acids |
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Where are amino acids stored in the body?
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NO SPECIFIC SITE.
They just form an amino acid pool (100g) instead of being stored away somewhere. |
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What does positive/negative nitrogen balance mean?
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In healthy adults, our nitrogen is constant. (intake = excretion)
Positive: Intake > Excretion (childhood, pregnancy --->any period of GROWTH really) Negative: Intake < Excretion (catabolic streess, starvation) |
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What's transamination?
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First step of amino acid catabolism.
Occurs in cytosol of most tissues. Amino group is removed from amino acid. Amino acid ----> alpha-ketoacid (using Aminotransferase as an enzyme) alpha-ketoglutarate + NH3 ----> Glutamate |
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What's Oxidative Deamination?
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Second step of amino acid catabolism.
Occurs in mitochondria of liver/kidney. Glutamate -----> alpha-ketoglutarate + NH3 (using glutamate dehydrogenase as an enzyme) |
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What are glucogenic alpha-ketoacids converted to?
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Pyruvate
or TCA intermediate |
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What are ketogenic alpha-ketoacids converted to?
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Acetyl CoA
Acetoacetyl CoA Acetoacetate |
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What are the ketogenic amino acids?
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Leucine
Lysine |
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How is ammonia transported to the liver?
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Within amino acids:
Glutamine ---> Glutamate + NH3 Alanine ----> Pyruvate + NH3 |
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Where does the urea cycle take place?
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Liver.
(mitochondria + cytosol) |
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What are the toxic effects of ammonia?
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Encephalopathy
Slurring Tremors Drowsiness Coma DEATH |
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Main causes of excessive ammonia?
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LIVER DAMAGE:
-Viral Hepatitis -Acute excessive alcohol abuse -Cirrhosis -Congenital |
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What's the name of the heel prick test?
And when is it performed? |
Guthrie Test
On, or after the 5th day of life |
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PKU is a deficiency of WHAT?
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Phenylalanine Hydroxylase.
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On a metabolic level, what's going on when someone has a deficiency of Phenylalanine Hydroxylase?
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PKU.
Phenylalanine cannot be converted to tyrosine. Phenylalanine builds up. Tyrosine is deficient. |
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Outcome of untreated PKU?
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Irreversible brain damage and mental retardation.
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How does albinism occur?
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Tyrosinase deficiency.
Tyrosinase converts: Tyrosine ---> Melatonin |
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How are PKU and MCAD acquired?
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Autosomal recessive disorders
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What do the following enzymes do?
i) Fructokinase ii) Phosphofructokinase |
i) Fructose ----> Fructose-1-Phosphate
(Fructose metabolism) ii) Fructose-6-Phosphate ----> Fructose-1,6-Phosphate (glycolysis) |
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What's the next stage after glyceraldehyde-3-phosphate (GAP) in glycolysis?
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----> 1,3-bisphosphoglycerate
NAD is reduced |
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What happens to 1,3-bisphosphoglycerate in glycolysis?
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-----> 3-phosphoglycerate
ADP ---> ATP |
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In glycolysis, what is converted to pyruvate?
And how? |
Phosphoenolpyruvate (PEP)
using Pyruvate Kinase (PK) ADP ----> ATP |
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What does Aldolase-B do?
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1. Fructose-1-phosphate ----> Glyceraldehyde (---> GAP)
2. Fructose-1-phosphate ----> DHAP |
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What does a deficiency in Fructokinase cause?
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Essential Fructosuria
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What is Essential Fructosuria?
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Deficiency of Fructokinase.
Hereditary benign condition. Symptomless. Fructose appears in urine. |
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What does a deficiency of Aldolase-B cause?
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Hereditary Fructose Intolerance.
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What is Hereditary Fructose Intolerance?
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Aldolase-B deficiency.
Severe inborn illness, appears in weaning. -Convulsions, excessive sleepiness, vomiting, irritability -Liver damage, jaundice, hypoglycaemia |
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How much glycogen is stored in the:
a. Liver b. Muscle |
a. 100g
b. 400g |
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What does insulin do to PDH, Acetyl-CoA Carboxylase and Fatty Acid Synthase?
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Activates.
(These enzymes are all used to convert glucose ---> fatty acids) |
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What type of bonds are in glycogen molecules?
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alpha-1,4 between monomers
alpha-1, 6 branches |
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Tell me the Lipolysis pathway:
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Triglyceride
l l <---- HSL V Monoglyceride + 2 fatty acids l l MAG LIPASE V 3 Fatty Acids + Glycerol |
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Name the fat soluble vitamins.
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A
D E K |
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Tell me about vitamin A:
(source, function and deficiency) |
Retinal (eye) pigment
found in meat/fish + carotenes Deficiency causes night blindness |
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Tell me about vitamin D:
(source, function and deficiency) |
Calcium absorption
Found in animal/fish fat And sunlight! Deficiency causes rickets and osteomalacia (soft bones in adults) |
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Tell me about vitamin E:
(source, function and deficiency) |
Antioxidant
Found in most foods Deficiency causes peripheral neuropathy |
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Tell me about vitamin K:
(source, function and deficiency) |
CLOTTING FACTORS: II, VII, IX, X
Found in plants Deficiency causes haemorrhagic disease |
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How are fat soluble vitamins absorbed?
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With micelles during fat absorption
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After lipolysis, what happens to the fatty acids?
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1. They are released into the blood, where they bind to proteins.
2. Taken up by liver + muscle cells. 3. Fatty Acid metabolism. (beta-oxidation) |
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After lipolysis, what happens to the glycerol?
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Oxidised and phosphorylated to DHAP.
----> Glycolysis! |
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fatty acid ---> fatty acyl CoA
what enzyme is involved? and where does this occur? |
Fatty acyl CoA synthase
ATP ----> AMP Cytosol of liver/muscle cell |
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What does micturition mean?
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Urination
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How does fatty acyl-CoA travel from the inter-membranal space of the mitochondria to the inner matrix of the mitochondria?
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Joins with Carnitine to form Fatty Acyl-Carnitine.
CPT1 enzyme used. |
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What happens to Fatty Acyl-Carnitine?
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Enters mitochondrial matrix.
Carnitine has finished its transportation job, so it interacts with CPT2 enzyme and leaves Fatty Acyl-CoA to venture off on its own. |
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Tell me about Beta Oxidation.
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Final stage of FA metabolism.
In the mitochondrial matrix, Fatty Acyl-CoA is converted to Acetyl-CoA. NAD + FAD are reduced. |
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SECRETIN: Tell me...
1. Stimulus for release 2. Site of release 3. Function |
1. Acidic chyme enters duodenum (Intestinal phase)
2. S cells in duodenum 3. -Stimulates bicarbonate (alkaline) synthesis + release from pancreas. -Inhibits gastrin release ---> reduces HCl production |
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What is the blood supply to the gallbladder?
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Cystic Artery
(from the right hepatic artery) |
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How can a defect in FA oxidation cause hypoglycaemia?
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The ATP generated in fatty acid oxidation supplies the ATP needed to activate Pyruvate Carboxylase for the following reaction:
Pyruvate ---> Oxaloacetate Without this reaction, gluconeogenesis cannot take place. |
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Causes of cirrhosis?
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ABC:
Alcohol B (Hepatitis) C (hepatitis) |
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Exocrine cells of the pancreas are named:
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Acinar cells
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The bare area of the liver is in contact with what organ?
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Right kidney
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Which amino acids are both glucogenic AND ketogenic?
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Tyrosine
Phenylalanine Isoleucine Tryptophan |
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What does lipoprotein lipase do?
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Breaks down the triglycerides in VLDL to 2 fatty acids + monoglycerol.
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How does the stomach develop?
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Fusiform dilation (4th week)
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Prenatal function of the liver?
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Haematopoesis
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What is an anion gap?
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Difference between anions and cations in the blood.
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What happens to the anion gap in MCAD?
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Elevated
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So, Acetyl-CoA is required for ketogenesis...
But where is this acetyl-Coa generated? (name 3 sources) |
1. Beta oxidation of fatty acids.
2. From pyruvate (glycolysis) 3. Catabolism of ketogenic amino acids |
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When are ketones synthesised?
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Conditions of:
1. High circulating fatty acids 2. Low insulin conc. (starvation, insulin) |
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Are ketones water or lipid soluble?
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Water
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What are the three ketones produced in ketogenesis?
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1. Acetoacetate
2. Acetone 3. Beta-hydroxybutyrate |
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Why is Phenylpyruvate not normally excreted in urine?
|
Phenylalanine is normally converted to Tyrosine, using phenylalanine hydroxylase.
However, when phenylalanine hydroxylase is absent, some phenylalanine is converted to phenylpyruvate (and phenylacetate + phenyllactate) instead. This is excreted in urine. |
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What colour hair and eyes do people with PKU tend to have?
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Fair hair, blue eyes.
(lack of tyrosine ---> lack of melanin) |
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Where is acetyl-CoA converted to ketone bodies?
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Liver mitochondria
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Where are ketones metabolised?
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Mitochondria of muscle and brain cells.
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What causes sweet breath in diabetics?
|
Acetone in the blood (product from ketogensis)
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KETOGENESIS:
Which enzyme converts acetoacetyl-CoA --> acetyl Co-A? |
Thiolase
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Tell me about Vitamin B1:
(source, function and deficiency) |
aka Thiamine
Source: Pulses + Pork! Function: Decarboxylation of pyruvate and alpha-ketoacids. Deficiency: Beri-Beri (cardiovascular + nervous symptoms) |
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Tell me about Vitamin B2:
(source, function and deficiency) |
aka Riboflavin
Source: Most foods Function: Flavin Nucleotides FAD + FMN Deficiency: Sore Mouth Normocytic Anaemia |
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Tell me about Vitamin B3:
(source, function and deficiency) |
aka Niacin
Source: Meat + Pulses/Grains Function: NAD + NADP Deficiency: Pellagra (skin lesions) Bowel, nervous, mental disorders |
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Tell me about Vitamin B6:
(source, function and deficiency) |
aka pyridoxine
Source: Most foods Function: Transamination in Amino Acid synthesis Deficiency: Skin lesions Convulsions |
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Tell me about Vitamin B12:
(source, function and deficiency) |
aka Cobalamin
Source: Animal Products only Function: Formation of RBCs Deficiency: Pernicious (Megabolatic) Anaemia (stored in liver ---> takes 1-3y for deficiency to show) |
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Tell me about Biotin:
(source, function and deficiency) |
Source: Liver, yeast
Function: Carboxylation Deficiency: Neurologic Changes |
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Tell me about Folic Acid:
(source, function and deficiency) |
Source: Greens, liver, yeast
Function: Synthesis of Purines + Thymine Deficiency: Megabolastic Anaemia |
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Tell me about Vitamin B5 (Pantothenic Acid):
(source, function and deficiency) |
Source: Most foods
Function: CoA Deficiency: "General Illness" |
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Tell me about Vitamin C:
(source, function and deficiency) |
aka Ascorbic Acid
Source: Fruit + Veg Function: Collagen synth. Deficiency: Scurvy! -bruising, bleeding, impaired healing |
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B vitamins are fat or water soluble?
|
Water
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Can water soluble vitamins be stored?
|
Nope.
Readily excreted in urine. |
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What substance, secreted in the stomach, is essential for Vit B12 absorption?
And what kind of cell secretes it? |
Intrinsic Factor.
Parietal Cells. |
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Which thyroid hormone is T4?
|
Thyroxine.
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Which thyroid hormone is T3?
|
Tri-iodothyronine.
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How do Iodide ions enter the thyroid cells?
|
1. Blood ---> Thyroid Follicular cell
Through Na+ / I- Symporter channels (NIS) 2. Thyroid Follicular Cell ----> Thyroid Through Pendrin transporter (PDS) |
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What's the name of the enzyme that oxidises Iodine in the thyroid?
|
Thyroid Perioxidase
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What happens to the Iodide ions after they have been oxidised?
|
Bind to thyroglobulin (Tg)
Tg then binds to either MIT/DIT to form T3/T4. |
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What happens to thyroglobulin (Tg) after being bound to oxidised iodine?
|
Either:
-Binds to MIT ----> T3 -Binds to DIT -----> T4 |
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How are T4 and T3 transported in the blood?
|
99% protein bound...
70% = Thyroid Binding Globulin (TBG) 20% = Albumin 10% = Transthyretin (TTR) |
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Half life of T4?
|
1 week
(large circulating plasma protein bound reservoir) |
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Half life of T3?
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1 day
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How is T4 converted to T3?
|
Deionidation in the liver / kidney
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Thyroid Stimulating Hormone (TSH) is also known as what?
|
Thyrotropin
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What does the hypothalamus release, with regards to the thyroid?
|
Thyrotropin Releasing Hormone (TRH)
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Where is TSH released?
And what stimulates its release? |
Anterior Pituitary (thyrotroph cells)
TRH |
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What stimulates T3 + T4 release?
|
TRH (hypothalamus) ---> TSH (ant. pituitary) ---> T3 + T4 (thyroid)
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Half life of TRH?
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3 mins
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What inhibits the secretion of TRH?
|
T3
T4 Dopamine |
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What two substances does TRH stimulate the release of?
And where from? |
TSH and Prolactin
Anterior Pituitary |
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What inhibits TSH release?
|
T3
T4 Dopamine Somatostatin |
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Half life of TSH?
|
1 hour
|
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What are the developmental actions of Thyroid hormone?
|
1. Bone Growth
2. Neurological: -Motor func. -Hearing -Intelligence -Speech + language |
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What does thyroid hormone do with regards to catecholamines?
|
Increases sensitivity to catecholamines
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What are the metabolic functions of thyroid hormone?
|
Regulates Basal Metabolic Rate
Thermogenesis Lipid Metabolism H2O/Salt balance Heart contraction Reflex times + muscle strength |
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Cretinism is caused by what?
And what are its symptoms? |
Untreated congenital hypothyroidism (Iodine deficiency)
Mental Retardation Growth Restriction Spastic Diplegia |
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Symptoms and signs of Hypothyroidism?
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Symptoms:
Sensitivity to cold, Fatigue Depression, Slower Cognition Menorrhagia, Anovulation Muscle weakness, constipation Signs: Bradycardia, Dry skin, Hair loss, cool extremities |
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Causes of Hypothyroidism?
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-Iodine Deficiency
-Autoimmune (Hashimoto's, Atrophic Thyroiditis) -Thyroidectomy -Secondary cause (eg. pituitary problem) |
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What is myxoedema?
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Severe, untreated hypothyroidism
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Symptoms of Hyperthyroidism?
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Weight loss
Intolerance to heat Anxiety, hyperactivity, insomnia, fatigue Palpitations Hair loss Tremor Increased bowel movement freq. |
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What foods is Iodine found in?
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Fish / seafood / seaweed
Milk |
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What is our daily iodine requirement?
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150 micrograms
(more in pregnancy) |
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In the liver, what is the lobe next to the gallbladder called?
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Quadrate
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What is the major difference between the mucosa lining the small and large intestines?
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The large intestine does not contain villi
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Why are people with Crohn's likely to have macrocytic anaemia?
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Crohn's can affect the terminal ileum, where B12 is absorbed.
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How long after a meal does insulin peak?
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30-60 mins
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Mechanism behind Coeliac disease?
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Gliaden (a prolamin) in gluten interacts with tissue transglutaminase, causing an inflammatory reaction which causes villous atrophy.
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What can large gallstones cause?
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Biliary retention
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Where are stem cells found in the colon?
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Bottom of the crypts of leiberkun
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What fuels can muscle use?
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Glucose
Fatty Acids Ketones |
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Goblet cells are found in the colon:
True or false? |
DAMN RIGHT THAT'S TRUE
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What channel lets glucose into the beta cells?
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GLUT2
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What inhibits insulin secretion?
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Adrenaline
Somatostatin |
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What kind of diarrhoea do Mg salts cause?
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Osmotic
(as Mg cannot be absorbed) |
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What kind of diarrhoea does lactolase cause?
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Osmotic
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What kind of diarrhoea do senna and castor oil cause?
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Secretory
as it is an irritant |
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Is segmentation propulsive?
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Nope. It's more like churning.
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How does epinephrine raise blood glucose?
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Inhibits insulin.
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4 possible causes of constipation?
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1. Reduced dietary fibre
2. Pregnancy (reduced smooth muscle contraction) 3. Aging (reduced muscle tone) 4. Psychological (depression, anorexia) |
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What are Incretins?
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GI hormones that stimulate insulin release.
2 main ones are: -Glucagon-like peptide 1 (GLP-1) -Gastric Inhibitory Peptide (GIP) |
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What are the minor stimuli for glucagon release?
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Cortisol
Stress Epinephrine Gut Hormones |
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What happens to proinsulin in the golgi?
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Cleaved to insulin and C-peptide
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What hormone inhibits both glucagon and insulin release?
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SOMATOSTATIN
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What enzyme inactivates the major incretins?
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Dipeptydyl peptidase-4
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In the fed state, muscle protein synthesis is
a. Less than b. More than c. Balanced by Protein degradation. (which letter is true?) |
C
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What is Maturity Onset Diabetes of the Young (MODY2) caused by?
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Gene defect.
No glucokinase can be made, so glucose cannot be converted to glucose-6-phosphate. |
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Insulin and glucagon...
which one inhibits which? |
Insulin inhibits glucagon.
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How much glucose is in the body?
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~5g
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Minor stimuli for insulin release?
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Cholinergic nerves (Ach)
Gut peptides Amino Acids |
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What does Somatostatin inhibit?
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EVERYTHING IT TOUCHES.
-EVERY GI hormone (gastrin, histamine, CCK, Secretin...) -TSH + Prolactin -Insulin AND glucagon -Growth hormone (it is officially the Voldemort of the hormones.) |
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In the intestines, where is potassium absorbed/secreted?
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Small: Absorbed
Large: Secreted |
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How and where is the pH microclimate formed in sodium absorption?
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Duodenum + Jejenum
Na ions are absorbed + exchanged for H+ ions. |
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Where are dietary proteins (well, amino acids) absorbed?
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Small intestine - jejenum + ileum
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What channel transports Di/tripeptides into enterocytes?
And what else goes through this channel? |
PepT1
H+ ions are absorbed with the di/tripeptides. And drugs! |
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NHE3 channel...
What does it do and where is it found? |
Sodium–hydrogen antiporter 3
Takes in Na+ Secretes H+ Found on basal membrane of enterocytes and in the kidney |
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PAT1 channel...
What does it do and where is it found? |
Intakes amino acids and H+ ions into enterocytes.
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How does the NHE3 channel cause amino acid absorption in the small intestine?
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It pumps out H+ ions in exchange for Na+ ions.
This creates a pH gradient (6 in the intestinal lumen, 7 in enterocyte), which drives diffusion of amino acids with Na+ and H+ back into the enterocyte. |
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What is the acidic microclimate of small intestine useful for?
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Amino acid absorption.
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Around 50% of amino acids/proteins are absorbed in what form?
And why? |
Di/tripeptides.
Kinetic advantage over individual amion acid monomer intake. |
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The PepT1 channel in small intestine absorbs something other than dietary amino acids and ions...
WHAT IS IT? |
DRUGS:
-ACE Inhibitors -Thrombin antagonists -Renin antagonists -Antibiotics -Antitumour agent -Prodrugs |
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How are ACE Inhibitors absorbed?
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Through PEPT1 channels in jejenum + ileum.
With amino acids and H+ ions. |
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What is Hartnup disease?
i. Type of disease/ cause: ii. Mechanism: ii. Signs / Symptoms: |
i. Autosomal-recessive disease, caused by defective amino acid absorption.
ii. Defect in System B (apical membrane) transporters ---> Neutral AAs (eg. tryptophan, ) cannot be absorbed (intestine) or reabsorbed (kidney). iii. Often asymptomatic. Neutral Aminoaciduria Can cause pellagra (as tryptophan is converted to niacin), diarroea + more... |
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What is Cystinuria?
i. Type of disease/ cause: ii. Mechanism: ii. Signs / Symptoms: |
i. Autosomal-recessive disease, causing defective amino acid absorption.
ii. Defect in System B0+ or b0+ apical membrane transporters. Cationic (basic) amino acids and cystine cannot be absorbed. Cystine cannot be reabsorbed in the kidney. iii. Cystine stones (kidney stones) in kidney, bladder, ureter, urine. |
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Certain genetic disorders mean that patients cannot absorb certain essential amino acids. This is due to defective amino acid transporters in the gut.
However, these disorders do not always result in a deficiency of amino acids. Why? |
50% of amino acids are absorbed as di/tripeptides, rather than as amino acid monomers.
In some cases, the transporter for amino acids is defective, but the amino acid can still be absorbed within di-tripeptides. |
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What is Lysinuric Protein Intolerance?
i. Type of disease/ cause: ii. Mechanism: ii. Signs / Symptoms: |
i. Autosomal-recessive disease, caused by defective amino acid absorption. Ver severe but only seen in about 100 people worldwide (half of whom are in Finland.)
ii. Defect in System y+L basolateral membrane transporter. Cannot absorb cationic AAs. iii. Vomiting, diarrhoea, coma when fed protein. -Arginine + Ornithine deficiency = restricted urea cycle ---> Hyperammonaemia! -Lysine deficiency = Skeletal + Bone abnormalities. (Dietary protein restriction + citrulline supplements are needed) |
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At what stage in the urea cycle is H20 converted to urea?
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Arginine ---> Ornithine
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Urea Cycle:
What two substances combine to produce Carbamoyle Phosphate? |
HCO3- + NH4+
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Urea Cycle:
Citrulline binds with aspartate to produce ______? |
Arginosuccinate
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Urea Cycle:
Arginosuccinate ----> Arginine What else is going on in this step? |
Fumarate leaves...
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Urea Cycle:
Ornithine binds with ______ to produce Citrulline? |
Carbamoyle Phosphate
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Urea Cycle:
Arginine ---> Ornithine ---> ...what happens next? |
Ornithine enters the mitochondria and binds to Carbamoyle Phosphate to produce Citrulline.
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What does the large intestine have instead of villi?
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Tubular secretory glands
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How is sodium absorbed in the duodenum/jejenum?
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Apical and basolateral Na/H-countertransporters contributing to the pH microclimate.
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How is sodium absorbed in the jejenum/ileum?
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Apical nutrient-coupled transporters (e.g. glucose).
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What is primary mechanism for Na+ absorption in the GI tract during the inter-digestive period?
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Na+/H+ exchange
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Fluid secretion in the GI tract is regulated by controlling Cl- section. What is required for Cl- to be secreted in to the lumen?
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Na+/K+/2Cl- co-transport across the basolateral membrane
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What is solute drag?
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The movement of a solute following bulk flow of solvent.
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In the GI tract, where does Cl- secretion occur?
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EVERYWHERE.
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K+ is absorbed somewhere by the paracellular route...
where is this somewhere? |
Distal small intestine
(jejenum/ileum) |
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In the intestines, where is K+ secreted?
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Large intestine
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In the intestines, where is K+ absorbed?
And how? |
Distal small intestine (paracellular route)
Distal large intestine (through K/H-countertransporters) |
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Na+
K+ H+ Cl- Which of the above is not secreted in the intestines? |
Na+
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Where is Cl- absorbed?
And how? |
1. Distal small intestine + Distal Large Intestine
(Passive paracellular and facilitated transcellular diffusion) 2. Ileum + Colon (Bicarbonate countertransport) |
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Cl- is absorbed along the entire intestinal tract, except one part...what is that part?
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Duodenum.
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Where is sodium absorbed?
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Every part of intestinal tract.
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Where, in the intestinal tract, is sodium secreted?
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Nowhere...
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There are 4 different ways that sodium is absorbed, in four different places.
Tell me about 'em. |
1. Duodenum + jejenum
-Apical and basolateral Na/H-countertransporters contributing to pH microclimate 2. Jejenum + Ileum Nutrient coupled absorption (so, with AAs + glucose) 3. Ileum + Proximal Colon Electro-neutral bicarbonate secretion 4. Distal Colon Electrogenic direct absorption (simple Na/K pump) |
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Where does Cl- absorption by the bicarbonate secretion process take place?
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Ileum + Colon (proximal + distal)
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Where does K+ secretion take place?
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Colon (proximal + distal)
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How are where is K+ absorbed in the large colon?
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H+/K+ countertransporter.
Distal colon. |
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Tell me whether K+ is absorbed/secreted in each of the following locations:
1. Proximal Small Intestine 2. Distal Small Intestine 3. Proximal Large Intestine 4. Distal Large Intestine |
1. Neither.
2. ABSORBED (paracellular) 3. SECRETED (paracellular + transcellular- using Na/K/2C pump) 4. ABSORBED (using H+/K+ pump) |
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What does the term "Secretagogue" mean?
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A secretagogue is a substance that causes another substance to be secreted.
(eg. gastrin, Angiotensin II) |
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Where is Intrinsic factor released?
And what does it do? |
Parietal cells
B12 absorption |
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What do Chief cells do?
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Release pepsinogen
(low pH) pepsinogen ---> Pepsin |
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Where are parietal, mucus, chief and ECL cells located?
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Corpus of stomach
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Where are the APUD cells of the stomach located?
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Antrum
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What is gastritis?
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Inflammation of stomach mucosa.
H+ irritates mucosa and activated immune mast cells. ---> releases mediators of inflammation (eg. Histamine) Local vasodilation ---> Increases blood supply which: Supplies more HCO3- Removes more H+ |
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Possible causes of Acute Gastritis?
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Drugs (eg. NSAIDs)
Alcohol Bacteria / toxins |
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Possible causes of Chronic Gastritis?
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Anything that causes continuous damage to mucosal lining...
-Helicobacter pylori -NSAID overuse -Pernicious anaemia (autoimmune attack of parietal cells) |
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What can Chronic Gastritis lead to?
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Stomach ulceration
Stomach carcinoma |
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In the GI tract, what is GALT?
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Gut Associated Lymphoid Tissue.
Found in Lamina Propria |
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What are the two nerve plexi in the GI tract walls called, and where are they located?
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1. Submucosal (Meissner's) plexus
in the submucosa 2. Myenteric (Auerbach's) plexus in between the circular and longditudinal muscle layers. |
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What three layers make up the mucosa layer of the GI tract walls?
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Epithelium
Lamina Propria Muscularis Mucosa |
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What are Interstitial Cells of Cajal?
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"Pacemaker" of the GI tract.
Generates slow phasic contractions of GI tract. 3/min in stomach 12/min in duodenum |
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Where are bile salts absorbed?
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Terminal Ileum
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Where is Vitamin B12 absorbed?
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Terminal Ileum
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Crohn's Disease:
i. What type of disease is it? ii. What's it caused by? iii. What are the symptoms? |
i. Type of inflammatory bowel disease.
ii. Autoimmune attack on the bowel causes inflammation of GI tract. Terminal Ileum is most often affected, though any area of GI tract (from mouth to anus) can be affected. iii. Abdominal pain Diarrhoea – may or may not be bloody Weight loss Fatigue ... |
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Crohn's Disease commonly leads to a deficiency in what?
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B12
Fat (and more, depending on the severity of the disease) |
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Why might Crohn's Disease lead to steatorrhoea?
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Impaired blie salt absorption ---> Impaired fat absorption
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Why might Crohn's Disease lead to gall stones?
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Reduced bile salt absorption ----> reduced bile acid reserve pool ---> less cholesterol held in micelles
---> cholesterol forms gallstones instead |
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What kind of anaemia is common in Crohn's?
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Pernicious (B12 deficiency)
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What type of cells release CCK?
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I cells (duodenum + jejenum)
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What effect do prostaglandins have on the GI tract?
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Reduces gastric acid secretion
Increases: -Blood flow to gastric mucosa -Mucus secretion -HCO3- secretion -Intestinal secretion |
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Where is Gastric Inhibitory Peptide (GIP) released from?
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K cells
(duodenum + jejenum) |
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Gastrin acts on which receptor on parietal and ECL cells?
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CCKB
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Ach acts on which receptor on parietal and ECL cells?
And what action does this have? |
M3
ECL: Histamine secretion Parietal: Activates H+/K+ channel ---> Acid secretion |
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How does Helicopbacter pylori survive in the acidic stomach environment?
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Burrows into gastric mucosa.
Uses urease to produce ammonia, which buffers acid. |
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Pharmacological control of gastric acid secretion:
Name me some H2 receptor antagonists. |
Cimetidine
Ranitidine |
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Pharmacological control of gastric acid secretion:
Name me a Ach receptor antagonist. |
Hyocine
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Pharmacological control of gastric acid secretion:
Name me a prostaglandin agonist. |
Misoprostol.
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Pharmacological control of gastric acid secretion:
Name me a Proton Pump Inhibitor. |
Omeprazole.
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What stimulates GIP (gastric inhibitory peptide) release?
And what does GIP do? |
Fat in the duodenum or ileum.
Inhibits gastrin and gastric acid secretion. |
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What stimulates VIP (Vasoactive Intestinal Peptide) release?
And where is it released from? And what does VIP do? |
Stomach distension.
Released from enteric nerve endings. Inhibits gastic acid secretion and relaxes stomach muscle. |
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Enteric nervous system:
What substances Increase [Ca2+]or cAMP in Crypt epithelia to increase Cl- transport? |
Secretagogues (e.g. Ach, 5-HT & VIP)
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Enteric nervous system:
What substances Decrease [Ca2+] and increase NaCl absorption? |
Enkephalins & norepinepherine
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What effect does Angiotensin II have on electrolyte absorption in the gut?
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Increases Na+ absorption (apical Na+/H+ exchange).
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What effect does Aldosterone have on electrolyte absorption in the gut?
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Increases Na+ absorption (ENaC & Na+/K+ ATPase)
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What effect does Somatostatin have on electrolyte absorption in the gut?
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Increases Na+ absorption [Ca2+]i and ↑ NaCl absorption.
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Where is guanylin secreted?
What does guanylin do? |
Secreted by goblet cells in the colon.
Increases Cl- secretion in the gut. Decreases water absorption. which causes diarrhoea. It does this to flush out pathogens. |
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Name three substances that reduce fluid absorption by increasing Cl- secretion in the gut.
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Guanylin
Prostaglandin (released when gut is inflamed) Histamine (from mast cells in lamina propria) |
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What do Inflammatory mediators such as NF-KB do to the epithelium of the intestine?
|
Increase permeability so that more fluid can pass into the lumen via the paracellular route.
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How do Cholera toxin and E. coli heat-labile toxin cause diarrhoea?
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(endocytosis) Activates Adenyl Cyclase
Increases cAMP Activates CFTR channels More Cl- secretion Less water absorption |
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How does E. coli heat-stable toxin (STa) cause diarrhoea?
|
Binds to guanylin receptor.
Activation of guanylate cyclase Increased cAMP More Cl- secretion Less water absorption |
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How does histamine reduce water reabsorption in the gut?
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Inflammatory response: Released from Mast cells in the lamina propria.
Travels along enteric nerves. Binds to H1 receptors on gut epithelial cells. Increases cAMP Increases Cl- secretion Reduces H2O absorption |
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Tell me.
What are four possible treatments for diarrhoea? |
1. Oral rehydration fluids
2. Absorbants - Kaolin (chalk). 3.Reduce motility -Opiates (e.g. loperamide). -Atropine. 4. Inhibit secretion -Opiates. |
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How much H2 gas does the body produce per day?
|
NONE.
H2 is produced by bacteria. |
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H2 breath test:
WHat does no increase in breath H2 after sugar ingestion suggest? |
Normal digestion / absorption of sugars
H2 producing colonic bacteria are not present |
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H2 breath test:
Rapid increase in breath H2 following sugar ingestion suggests ...? |
o Fast oro-caecal transit time
o Bacterial overgrowth or intestinal diverticulum |
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H2 breath test:
Delayed increase in breath H2 following sugar ingestion suggests...? |
Non-absorbable carbohydrates have reached the caecum
Incomplete digestion/absorption of sugar |
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What do opiates and anti-cholinergics do to gut transit time and gut motility?
|
Increase transit time
Decrease Gut motility |
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What do pro-kinetics do to gut transit time and gut motility?
|
Reduced transit time
Increase gut motility |
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What two general things is the H2 breath test excellent at detecting?
|
Defects in sugar absorption/digestion
Bacterial overgrowth in small intestine |
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What is Zollinger–Ellison syndrome?
|
Gastrin-secreting tumour causes excessive gastric acid secretion.
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What level is the Coeliac trunk at?
And what does it supply? |
T12
All foregut derivatives: Oesophagus Stomach Upper duodenum Liver, gallbladder Pancreas |
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What level is the Superior Mesenteric Artery at?
And what does it supply? |
L1
Midgut derivatives: Lower duodenum to the right half of transverse colon. |
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What vertebral level is the Inferior Mesenteric Artery at? And what does it supply?
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L3
Hindgut derivatives: Left half of transverse colon and beyond! |
