diabeetus Flashcards
T1DM overview, RF, Differential diagnosis.
destruction of Beta cells of pancreas- occurs in genetically susceptible individs with environmental trigger. T4 hypersensitivity (delayed T cell mediated)
often presents with diabetic ketoacidosis.
Risk factors: fam member with T1DM, autoimmune thyroid dis, coeliac dis, pernicious anaemia. ‘clean’ environment as a child.
differentials- alcoholic ketoacidosis (body has to break down FA as 1st gluconeogenesis stop is blocked) - normal to low glucose sign.
S+S of T1DM + pathophys + IX.
S+S: hyperglycaemia without ketoacidosis, polyurea, ploydipsia, wt loss. Ketonurea, weakness, N+V, cramps, blur vision, abdo pain, dehydration, tachycardia, DKA.
Lack of insulin => high glucose levels => high osmolality of blood => body thinks you are ‘dehydrated’ => polydipsia
High osmolality => body will secrete lots of aldosterone + ADH
Lack of insulin => glucose cannot enter cells => body thinks you are being starved => mobilisation of lipids
Fatty acids are converted to ketones
insulin affects GLUT4 receptors, found on skel muscle and fat cells + heart.
Baseline bloods => FBC, U+E, laboratory glucose
HbA1c => see below
TFTs and TPOs to test for associated autoimmune thyroid disease
Anti-TTG for associated coeliac disease
Insulin antibodies, anti-GAB and islet cells antibodies
C-peptide
discuss Hba1c and other forms of glucose monitoring
HBA1C- glycated haemoglobin- how much glucose is attached to the haemoglobin in the RBC. considered an avg over last 3/12 (RBC last 3/12)
capillary- the classic
flash glucose- the little arm thing. measures glucose in interstitial fluid. 5min delay vs blood. spenny
management of T1DM.
long acting background insulin- OD typically evening.- Lantus
short acting- 30 mins before carb intake- Actrapid. (Subcut)
can use insulin pump- prov different rates of infusion, must be, diff controlling HBA1C. - can help control, can be diff to use the pump.
DKA synopsis, risks of hyper/po kalaemia
Acute, life threatening,. excessive ketogenesis due to no glucose in cells.
acetone is what you can smell.
causes acidosis (metabolic). often triggered by illness- reduce as lost appetite, but need 25% more as body is in catabolic state.
glucose >11.1.
dehydration, lots of glucose, SGLUT2 in kidney gets saturated, lots of glucose in the renal tubule, osmotic gradient changes, water is pulled into the tubule (less reabsorption)
metabolic acidosis => High H+ in serum => H+ goes into cells, K+ leaves cells => this can lead to vomiting, but can K+ is lost in urine
Note that DKA patients, for this reason, are at risk of both hypokalaemia and hyperkalaemia
Initially they are often hyperkalaemic (as lack of insulin so K+ cannot enter cells)
It can then be lost in urine => hypokalaemia
vomiting, confusion, coma, kidney damage (dec perfusion, inability to excrete hydrogen + ketones). hyperventilation (blow off acid)
severe DKA criteria and DKA management generally
ketones over 6.
bicarb <5.
ph <7.1
hypoK < 3.5
GCS 12, Spo2 92%.
Mx: ABCDE
2 cannulas- one for IV, one for Fluid.
NaCl + 20mmK 1L 2 hrs. 1L over 4 hrs (check K at this point). 1L over 8.
if K+ 3.5-5.5 40mm/L K. if less than 3.- seek help.
fixed rate insulin infusion- 0.1unit/kg/hr. continue with long acting insulin.
once glucose is less than 15- change NaCl to Dextrose to avoid hypo. all else the same.
aim for ketone reduction of 0.5 mm/l/hr.
T2DM overview S+S, RF,
insulin resistant due to metabolic syndrome.
insulin sensitivity defined as rate at which plasma glucose decreases per unit increase in plasma insulin.
RF: South asian, obesity, fam history, underactivity, low birth weight and low wt at 12. (low wt–> malnutrition which impairs beta cell development)
Weather- ginetic
when- lifestyle.
S+S: polyuria (gluc exceeds renal threshold), thirst, wt loss (fluid depletion, breakdown of fat).
lethargy, visual blurring, freq infections (UTI), loss of sensation, wt loss, Erectile dysfunction.
what are signs of insulin resistance (T2DM)
Acanthosis nigricans–> dark coloured skin, around neck and in the axillae, skin tags, central obesity, hirsutism.
pathophysiology of T2DM
normal: insulin binds receptor–> phosphorylation cascade–> GLUT4 expression–> glucose taken up into muscle and adipose tissue.
pathological state- Serine phosphorylation instead–> reduction in GLUT4. (never complete resistance obs)
as a result beta cells try and secrete more insulin- desensitising GLUT4 further.
at a certain point- glucose levels toxic to pancreas- beta cell destruction and insulin drops.
T2DM Ix + screening
HbA1c. must be more than 6.5% on at least 2 occasions is asymptomatic. (complications can be prevented with <7%)- cant be use in pregnancy- bleeding ulcer, splenectomy (lots of things- anything with bleeding- higher turnover of RBC)
random glucose- if higher than 11.1 on 2 occasions.
oral glucose tolerance- 75g of glucose in 300ml. bloods before drank and 2hrs later. if 11.1 or more- diagnostic. (7.8-11 is pre-DM)
fasting- >7 DM. 5.5-6.9- impaired fasting gluc. - 2 readings.
everyone over 40- questionaire + stratification. high risk 1-5 years hba1c.
management of T2DM
lifestyle interventions- low sugar carbs, high fibre, starch, low fat. 30 mins exs 5x a week.
Or
Lifestyle + metformin
Or
Lifestyle + metforin + 2nd drug agent (if HBA1C >8.5 @ diagnosis.
Equivalent of DKA but for T2DM
hyperosmolar hyperglycaemic state
glucose >33. no ketones, no acidosis.
hyperosmolar serum (2Na + 2K + glucose + urea)
pres: dehydration, vom, confusion, hyperglycaemia (polyuria, dypsia, phagia, seziures)
Rx: HDU/ITU. Reduce glucose (insulin), remove cause, fluid/ electrolyte balancing. 0.9% NaCl over 1-2 hours 15-20 ml/kg/hr
increases CVS events significantly. V dehydrated, VTE likely.
causes: high sugar, infections, steroid use, MI.
diabetic nephropathy pathophysiology.
pathology: excess glucose in blood sticks/ causes hardening/ stiffening/ narrowing of efferent arteriole in glomerulus.
This increases pressure in glomerulus- causing hyper filtration. Increased GFR at this point.
hyperfiltration causes damage- expansion of spaces (podocite slits) –> proteinurea.
in compensation- cytokine prod, inflammation. Mesangial cells expand + secrete more matrix –> glomerulus expands and hardens –> glomerular sclerosis –> decreasing GFR.
Macula densa thinks low BP due to the filtration and constriction. releases Renin + RAAS cascade. –> perpetuating CKD.
diabetic nephropathy S+S, Rx
increased gfr, proteinuria, decreased gfr.
Rx: treat the diabetes.
ACE inhibitors- will vasodilate the efferent arteriole (good for prophylaxis also)
discuss DM1 management before, during, and after surgery
DM1: night before- reduce long acting by 1/3 (or 25% some sources).
omit morning insulin + commence IV variable rate
whilst NBM 5% dextrose 125ml/hr. BM 2 hrly.
aim to keep BM less than 10mm/L during op, if short op can be managed with rapid subcut injection.
once E+D normal mgt can be continued.
MUST overlap IV and subcut insulin by 2-3 hours due to short half live of IV.
do not delay urgent surgery for HBa1C measurements, but consider if elective and hba1c is higher than 10%.
