anything else from the lectures worth knowing Flashcards by HARRY RICHARDSON

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

ketone bodies

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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

mobilises stored glucose into the blood

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by product of insulin processing

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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insulin receptro made of

if they are removed what happens

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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metabolic consequences of uncontrolled diabetes

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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diabetes is fasting glucose above

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diabetes is 2hr plasma glucose above

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define both type 1 and 2 diabetes mellitus

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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what do epsilon cells release

gherlin

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what do pp cells release

pancreatic polypeptide

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

type 1

cytotoxic cells seen
CD45 marker

symptoms start stage 3 - Honey moon stage

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4Ts of type 1

toilet
thirsty
tired
thinner

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do glucose levels increase when ketone levels increase

yes

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normal blood ketone level and level over which DKA is suggested

0.6mmol/L

above 3.0mmol/L

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what cytokines found in inflammation in insulin resistant states

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

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what are incretins

hormones produced by gut after food

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

type 2 diabetes

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complications

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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what is gestational diabetes

insulin resistance during pregnancy risk to mother and kid

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metabolic defect underlying type 2 is a triad of what

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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what cancers are linked with diabetes

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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falciform ligament contains what

obliterated umbilical vein

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what vessels split the lobes of the liver

hepatic veins

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pre hepatic causes of jaundice

haemolytic anaemia - raised bilirubin

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hepatic causes of jaundice

cirrhosis and acute hepatitis

obstruction or pot hepatic causes of jaundice

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

what test can you do to look at gallbladder

MRCP - magnetic resonance cholangiopancreatogrpahy

what is a stricture

an area of narrowing in the intestines

ERCP – endoscopic retrograde cholagnio pancreatography advantages

biopsy possible stent sphincterotomy PTC - percutaneous trans hepatic cholangiography

where does the pancreas lie in the human body

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

what does somatostatin do to insulin and glucagon secretions

reduces them

what cells release pancreatic enzymes

acinar cells

what do duct cells contain

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

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

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

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

secretin

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

CCK

EPI symptoms

steatorrhea - excessive undigested fat in faeces so floats malnutriton diarrhoea abdo cramps

treatment fro EPI

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

caused of EPI

CF chronic pancreatitis pancreatic cancer

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

yes

pancreatitis

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

most common pancreatic cancer

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

dyslipdemia

abnormal levels of cholesterol T! - thin at diagnosis

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

visceral WAT

what is retinopathy

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 )

how often do diabetics get screening for their eyes

every year prevention glcuose control BP control lipid control

treatment fro retinopathy

laser photocoagulation and anti-VEGF injections

how do you test for diabetic nephropahty

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

how often do we screen for retinopathy

annually

how to prevent nephropahty

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

what do ACEi do

dilate efferent as well as afferent glomerular arterioles

how often is diabetic food screened and check ed for

every year clinical skills

what medication do you use to treat gout

allopurinol

what surgeries reduce the amount of body fat

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 ```

stereotypes

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

prejudice

emotional reaction to someone on basis of group membership | Eg people with obesity disgust me

discrimination

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

weight bias

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

institutional bias

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

first line

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

what does metfromin do

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

what diabetic drugs cause weight loss

SGTL2

what medications cause weight loss

GLP-1

anything else from the lectures worth knowing Flashcards

(63 cards)