anything else from the lectures worth knowing Flashcards
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
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
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
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
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
diabetes is fasting glucose above
7
diabetes is 2hr plasma glucose above
11
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
what do epsilon cells release
gherlin
what do pp cells release
pancreatic polypeptide
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
4Ts of type 1
toilet
thirsty
tired
thinner
do glucose levels increase when ketone levels increase
yes
normal blood ketone level and level over which DKA is suggested
0.6mmol/L
above 3.0mmol/L
what cytokines found in inflammation in insulin resistant states
TNF alpha, IL-6 and IL-8 alter gut microbiota interupt
what are incretins
hormones produced by gut after food
what diabetes over 40 gradual onset insulin resistance very strong family history
type 2 diabetes
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
what is gestational diabetes
insulin resistance during pregnancy risk to mother and kid
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
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
falciform ligament contains what
obliterated umbilical vein
what vessels split the lobes of the liver
hepatic veins
pre hepatic causes of jaundice
haemolytic anaemia - raised bilirubin
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
