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metabolism > anything else from the lectures worth knowing > Flashcards

anything else from the lectures worth knowing Flashcards

1
Q

glucose is used to make ATP and is the primary metabolic source of the brain. What else can the brain use in glucose deficiency

A

ketone bodies

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2
Q

insulin is required to drive glucose uptake in muscles and regulate root of glucose metabolism but not uptake in the liver
what does glucagon do

A

mobilises stored glucose into the blood

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3
Q

by product of insulin processing

A

c-peptide wich is a metabolcilaly inaktive but a marker of insulin presence - this is how you check for an overdose

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4
Q

insulin receptro made of

if they are removed what happens

A

2 outer alpha units
2 beta units on the cell membrane

loss of receptors leading to resistance and loss of sensitivity - T2DM - so glucose accumulates in blood and lost in the kidneys

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5
Q

metabolic consequences of uncontrolled diabetes

A

loss of glucose
excessive fatty acid breakdown
ketone body production
carboxylic acid production leading to lower ph or acidosis or ketoacidosis

unquenchable thirst and nerve ceasing urinatioj

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6
Q

diabetes is fasting glucose above

A

7

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7
Q

diabetes is 2hr plasma glucose above

A

11

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8
Q

define both type 1 and 2 diabetes mellitus

A

Type 1 – insufficient insulin – beta cells killed by the immune system so less insulin made so less insulin to allow less glucose in

Type 2 – plenty of insulin – insulin ressitance – defect in signalling to GLUT4 moleue so less glucose uptake occurs

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9
Q

what do epsilon cells release

A

gherlin

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10
Q

what do pp cells release

A

pancreatic polypeptide

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11
Q 
what diabetes 
under 30 
rapid onset 
underweight 
ketoacidois 
autoantibodies ICA, GAD-65, IAA 
genetic predisposition
A

type 1

cytotoxic cells seen
CD45 marker

symptoms start stage 3 - Honey moon stage

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12
Q

4Ts of type 1

A

toilet
thirsty
tired
thinner

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13
Q

do glucose levels increase when ketone levels increase

A

yes

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14
Q

normal blood ketone level and level over which DKA is suggested

A

0.6mmol/L

above 3.0mmol/L

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15
Q

what cytokines found in inflammation in insulin resistant states

A

TNF alpha, IL-6 and IL-8 alter gut microbiota interupt

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16
Q

what are incretins

A

hormones produced by gut after food

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17
Q 
what diabetes 
over 40 
gradual onset 
insulin resistance 
very strong family history
A

type 2 diabetes

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18
Q

complications

A 
Diabetic complications
Microvascular complication – affecting smaller blood vessel s
-	Retinopathy 
-	Neuropathy 
-	Nephropathy 
Macrovasucalr complciations 
-	Stroke
-	Cardiomyopathy 
-	Peripheral vascular disease reducing the blood flow 
-	Diabetic foot 
Diabetic complications 
-	Angina 
-	MI 
-	HF
-	Stroke
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19
Q

what is gestational diabetes

A

insulin resistance during pregnancy risk to mother and kid

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20
Q

metabolic defect underlying type 2 is a triad of what

A

Metabolic defect underlying type 2 are a triad of insulin resistance, beta cell dysfunction and impaired hepatic glucose production.

Diabetic nephropathy – glomerular damage
Diabetic retinopathy – growth of abnormal blood vessels
Immune system is suppressed in type 1 so more susceptible to repsriatory infection eg pneumonia

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21
Q

what cancers are linked with diabetes

A

Stomach and cervical cancer with type 1

Type 2 – pancreatic , liver nd endometrial cancer
Colorectal baldde rna dbreast and non hodkins lyphome a
Reduces protse cancer risk

largest biggest cause of end stage renal failure

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22
Q

falciform ligament contains what

A

obliterated umbilical vein

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23
Q

what vessels split the lobes of the liver

A

hepatic veins

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24
Q

pre hepatic causes of jaundice

A

haemolytic anaemia - raised bilirubin

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25
Q

hepatic causes of jaundice

A

cirrhosis and acute hepatitis

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26
Q

obstruction or pot hepatic causes of jaundice

A

stones, strictures , cholangiocarcinoma, head of the pancreas cancer or hepatocellualr carcinoma

27
Q

what test can you do to look at gallbladder

A

MRCP - magnetic resonance cholangiopancreatogrpahy

28
Q

what is a stricture

A

an area of narrowing in the intestines

29
Q

ERCP – endoscopic retrograde cholagnio pancreatography

advantages

A

biopsy possible
stent
sphincterotomy

PTC - percutaneous trans hepatic cholangiography

30
Q

where does the pancreas lie in the human body

A

the pancreas lies under the liver and behind the stomach in the upper abdomen

31
Q

what does somatostatin do to insulin and glucagon secretions

A

reduces them

32
Q

what cells release pancreatic enzymes

A

acinar cells

33
Q

what do duct cells contain

A

sodium bicarb

carbonic anhydrase dissociates and sodium ions removed by hydrogen and bicarb transported in

34
Q

enterokinase(in mucosa) activates trypsinogen to converted to trypsin( and the chymo version) what activates procarboxypeptidase to carboxypeptidase

A

trypsin

pancreatic lipase only enzymes throughout the entire digestive system that can digest fat

35
Q

what hormone activated by the acid in the duodenum caused the duct cells to release alkaline solution

A

secretin

36
Q

when fat and protein are in the duodenal lumen what is released from duodenal mucose to act on the acinaar cells to secrete pancreatic digestive enzymes

A

CCK

37
Q

EPI symptoms

A

steatorrhea - excessive undigested fat in faeces so floats

malnutriton
diarrhoea
abdo cramps

38
Q

treatment fro EPI

A

pancreatic enzyme replacement therapy administered with meals and snacks

food that difficult to digest should be avoided

fat soluble vitamins such as zinc and selenium should be assessed

39
Q

caused of EPI

A

CF
chronic pancreatitis
pancreatic cancer

40
Q

in CF, Bicab secretion in ductal cell depends on protein CFTR
CFTR is both chloride channel and bicarbonate channel
When CFTR protein is defective, the secretion of bicarb by duct cells is decreased. leads to blockage in pancreatic ducts and inappropriate zymogen activation causing damage to acinar cells and duct cells.
CF normal with EPI is there a partial affect

A

yes

41
Q

pancreatitis

A

autodigestion by inappropriately activated pancreatic enzymes

2 forms are acute and chronic ( exocrine pancreatic parenchyma leading to fibrosis- most common cause is long term alcohol abuse)

digestive enzymes do not reach the duodenum leading to incomplete digestion

42
Q

most common pancreatic cancer

A

ductal adenocarcinoma

Adeno means in the lining

leading to enzymes not reaching duodenum and then enzymes secreted in pancreas leading to panreatisi and pain

most diagnosed at a relatively late stage

43
Q

dyslipdemia

A

abnormal levels of cholesterol

T! - thin at diagnosis

44
Q

what type of linked to developing T2DM and its co-morbidities

A

visceral WAT

45
Q

what is retinopathy

A

micro aneurysm and hard exudates start, circinate hard exudates form ,blot haemorrhages close to the macula, cotton wool spots and deep intra-retinal haemorrhages and new vessels form. However these vessels are fragile and can lead to pre-retinal haemorrhage or vitreous haemorrhage ( all red )

46
Q

how often do diabetics get screening for their eyes

A

every year

prevention
glcuose control
BP control
lipid control

47
Q

treatment fro retinopathy

A

laser photocoagulation and anti-VEGF injections

48
Q

how do you test for diabetic nephropahty

A

urine albumin - test ACR - detects early albumin - little point testing in advanced ( late is eGFR and serum creatinine)

albumin creatinine ratio

49
Q

how often do we screen for retinopathy

A

annually

50
Q

how to prevent nephropahty

A

BP control
glucose control
RAS blockade - ACEi or ARB - 1st line for hypertension in diabetes

51
Q

what do ACEi do

A

dilate efferent as well as afferent glomerular arterioles

52
Q

how often is diabetic food screened and check ed for

A

every year

clinical skills

53
Q

what medication do you use to treat gout

A

allopurinol

54
Q

what surgeries reduce the amount of body fat

A

Bariatric and metabolic surgery 0 roux on y gastric(RYGB), vertical sleeve (VSC) , LAGB , biliopancreatic diversion (BPD)

diets 
CICO – calorie sin calories out 
Low GI 
Low carb <130g/day <26% 
Low carb high fat 
Keto diet 
5:2 diet 
Intermittent fasting
55
Q

stereotypes

A

cognitive expectations and associations about groups of other people eg all people with obesity lack self-control

56
Q

prejudice

A

emotional reaction to someone on basis of group membership

Eg people with obesity disgust me

57
Q

discrimination

A

acting on the basis of stereotypes and prejudice, denial of equality of treatment (=biased behaviour)
Eg denying people surgery on the basis of their weight, behaviours etc eg fat shaming

58
Q

weight bias

A

negative attitudes or stereotypes people hold against people with obesity, and resulting discrimination/prejudice

59
Q

institutional bias

A

Institutional bias – equitable treatment regardless of race, ethnicity etc. is a patient right
This refers to accessibility of healthcare opportunities

explicit - conscious , implicit - unconscious

60
Q

first line

A

metformin
T1 insulin not produced so need to replace background with meal insulin
T2 can make own insulin so aim to make this insulin secretion more effective or increase supplant. Own insulin acts as a buffer

61
Q

what does metfromin do

A

reduces hepatic gluconeogenesis and is an insulin sensitiser

Begin at 500mg od increase by 500mg per week or after side effects
Aim for max dose 2000mg daily or 1000mg bd
If not tolerated use slow release

62
Q

what diabetic drugs cause weight loss

A

SGTL2

63
Q

what medications cause weight loss

A

GLP-1

metabolism (17 decks)

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