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Diabetes Flashcards

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1
Q

What is diabetes mellitus?

A

genetic predisposition and an autoimmune process causing gradual destruction of the beta cells of the pancreas, leading to no insulin production

deficiency or deminished effectiveness of endogenous insulin, hyperglycemic, deranged metabolism and causing microvascular problems

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2
Q

What are the different types of DM?

A

type 1 - failure to produce sufficient insulin
type 2 - the body’s resistance to insulin
gestational - high blood glucose levels during pregnancy, causing risk to mother and foetus
maturity onset diabetes of the young - monogenetic defects of B cell function (impaired insulin secretion), appearing as mild hyperglycaemia at a young age, autosomal dominant
secondary - from pancreatic disease,cystic fibrosis, cushing’s, acromegaly, thiazide diuretics, corticosteroids, congenital lipodystrophy, acanthosis nigricans, wolframs syndrome

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3
Q

What is the pre diabetic phase?

A

where auto immunity has been developed but no clinically apparent insulin dependency, insulin autoantibodies can be developed in genetically predisposed

triggered by viruses, dietary factors, enviromental toxins, emotional or physical stress, early cessation of breast feeding

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4
Q

Risk factors for type 1 diabetes?

A

10% have family history, associated with HLA DR3 and DR4 and islet cell antibodies, Caucasian, North Europe, Scandinavian, 30-50% concordance in twins, associated with other auto immune disease, eventual dissapearnace of C peptide, 6q determines islet sensitivity to damage

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5
Q

At what age does type 1 DM usually present itself?

A

juvenile onset, but can occur at any age

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6
Q

When does type 2 DM usually occur?

A

over 30, but becoming increasingly common in children and adolescents, polygenic disorder

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7
Q

Risk factors for type 2 DM?

A

excess body weight, physical inactivity, alcohol, south asia, history of gestational diabetes, impaired glucose tolerance, impaired fasting glucose, drug therapy, low fibre, hyglycaemic index diet, metabolic syndrome, polycystic ovarian syndrome, family history, male, elderly

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8
Q

Pathophysiology of type 2 DM?

A

the genetic form has mutations of the insulin receptor and structural alterations of the insulin molecule so patients gradually become insulin resistant and beta cells fail to secrete enough insulin and beta cell mass is reduced to 50% of normal, the C peptide persists

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9
Q

How do all DM present?

A

polyuria, polydipsia, lethargy, boils, glycosuria, blurred vision, thirst, signs of micro and macrovascular disease, pruritus, frequent and recurrent infections

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10
Q

Symptoms only in type 1 DM?

A

weight loss, dehydration, ketonuria, acetone breath, Kussmaul breathing, nausea, vomiting, hyperventilation, acute with short duration of symptoms

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11
Q

Symptoms only in type 2 DM?

A

acute and chronic complications, subacute with a longer duration of symptoms

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12
Q

Diagnosis of DM?

A

2 fasting venous plasma glucose - >7mmol/L
random plasma glucose and symptoms >11.1mmol/L
HbA1c >6.5% (48mmol/mol)
Fasting plasma glucose 11.1mmol/L
impaired fasting glucose 5.6-6.9mmol/L

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13
Q

Management of DM?

A

educate, self management, healthy diet, weight loss, smoking cessation, regular exercise, low sugar, high starch, glucose control, glucose and HbA1c monitoring, early detection, monitor complications, global assessment of cardiovascular risk, antidiabetic agents

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14
Q

Treatment of type 2 diabetes?

A

oral hypoglycemic agents, along with diet and lifestyle changes to get good glyaemic control

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15
Q

Function of insulin?

A

regulated carb and fat metabolism affecting the liver, muscle and fat tissue, causing glucose uptake

inhibits the release of glucagon and blocks fat being used as an energy source

stores excess energy

promotes the uptake of glucose from the blood into the liver and the conversion of glucose into glycogen and glucose to acetyl coA to triglyceroles into VLDL to be stored triglycerol in adipose tissue

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16
Q

Where is insulin synthesized?

A

in the pancreas, in the beta cells of the islets of Langerhan

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17
Q

What is insulin synthesized from and how?

A

synthesized from the preproinsulin, moves into the endoplasmic reticulum and then converted into proinsulin precursor by proteolytic enzymes known as prohormone convertases and exoprotease carboxypeptite E

splits the proinsulin precursor into A, B and C, A and B are joined by diastole bonds to make insulin and the C peptide helps G protein membrane

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18
Q

When is insulin released?

A

in response to increased blood glucose levels and then it is sustained with the slow release of newly formed vesicles, triggered independently of sugar

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19
Q

What stimulates insulin release?

A

GLUT 2 carries glucose into the beta cells, stimulating insulin release

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20
Q

How does insulin affect amino acids?

A

uptake of amino acids from the blood stream to the liver

then causes proteinogenesis and protein synthesis

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21
Q

How does insulin affect fat?

A

promotes storage of fat in skeletal muscle as fatty acids

synthesis of triglycerol

stores excess energy

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22
Q

What is the insulin receptor?

A

a tyroxin kinase receptor made up of 2 beta, 2 alpha and 2 tyroxin kinase (an enzyme which is usually inactive) subunits

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23
Q

When does tyroxin kinas become active?

A

when it has a phosphate group coming off it

insulin binds to the alpha subunits of the insulin receptor, causing the tyroxin kinase to become phosphorylated to be activated

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24
Q

What happens when the insulin receptor (tyroxin kinase) is activated?

A

intracellular effects of insulin occur from IRS-1 stimulation

promotes growth, gene expression, glycogen synthesis, fat synthesis, protein synthesis, increased glucose transporter expression (GLUT2 in liver and GLUT4 in muscle), so there is an uptake of glucose into the liver

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25
What causes insulin resistance?
insulin cannot bind to tyroxin kinase receptor so there is not an increase of GLUT2 receptors so glucose remains in the blood steam
26
What happens to glucose in the liver?
stored as glycogen or converted to fats and turned into VLDLs and transported into adipose tissue
27
How does insulin affect blood glucose levels?
decreases them
28
What effect does insulin have on enzymes?
inhibits glycogen phosphorylase into glucose and then promotes hexokinase and glycogen synthase to form glycogen, increased glucose transporters to liver and muscle, stimulate ribosome activity to make proteins and inhibits protein degradation and increase glycolysis for fat synthesis, and prevents beta oxidation
29
After lifestyle changes, what is the first medication used for type 2 diabetes treatment and how does it work?
Biguanides e.g. metformin - phosphorylates GLUT4 to increase glucose transport uptake and reduces glucose production from the liver, sensitizing target tissues to insulin
30
Why is metformin more effective in type 2 diabetes, and only used in type 1 if overweight?
it can only act in the presence of endogenous insulin so needs residual functioning pancreatic islet cells
31
Benefits of metformin?
reduces macrovascular complications and death, fewer hypoglycaemic attacks then sulphonylureas, does not cause weight gain, can be used in combination
32
Risk of metformin?
can cause lactic acidosis, has GI side effects at higher doses (nausea, vomiting, anorexia), an insulin secretagogues and has drug interactions with ACE-I, alcohol, NSAIDs, steroids and contrast agents
33
Who is most at risk of lactic acidosis in metformin use?
renal insufficiency, CV disease, PVD, liver disease, pulmonary disease, >65
34
What is the second line medication that can be used for type 2 diabetes treatment and how do they work?
Sulphonylureas e.g. glipizideare - block potassium channels on cell membrane, increasing pancreatic islet cell function opens calcium channels, increasing fusion of insulin granulae with the cell membrane to increase insulin release stimulates glycolytic pathway in the liver and inhibits glucose production
35
Benefits of sulphonylureas?
last 12-24hrs, good if metformin is CI, reduced glycosylated Hb (HbA1c) over a ten year period
36
Risks of sulphonylureas?
hypoglycaemia, weight gain, liver dysfunction, GI disturbance, CI in renal failure, hepatic failure, porphyria, pregnancy, breast feeding, drug interactions with ACE-I, alcohol, NSAIDs and steroids
37
In who is hypoglycaemia from sulphonylureas most common?
older age, mild-moderate hepatic impairment, renal impairment
38
How can hypoglycaemia be reduced in sulphonylurea use?
use a short acting drug like tolbutamide
39
How do rapid acting insulin secretagogues treat type 2 DM?
they are post prandial glucose regulators e.g. repaglinide and nateglinide - block potassium channels on pancreatic beta cells, stimulating insulin release, short acting
40
Benefits of rapid acting insulin secretagogues?
short duration and rapid onset repaglinide is better for irregular meal times and for poor glycaemic control and target post prandial hyperglycaemia nateglinide is used with metformin and is a sulfonylurea receptor binder given before meals
41
Risks of rapid acting insulin secretagogues?
hypoglycaemia, weight gain, CI in hepatic failure, pregnancy and weight gain, drug interactions with ciclosporin, trimethoprim and clarithromycin
42
What is the third medication given in type 2 DM treatment and how does it work?
Thiazolidinediones (TDZs)/glitazones e.g. pioglitazone - activates nuclear peroxisome proliferation activated receptor (PPAR) which regulates genes that influence insulin sensitive genes to enhance production of mRNAs of insulin dependent enzymes and increasing hepatic sensitivity to insulin, enhancing glucose clearance
43
Benefits of TDZs?
used in combination with S or M, TDZ with M is good for obese patients but can cause deterioration of blood glucose control pioglitazone can be used with insulin therapy if this happens
44
Risks of TDZs?
weight gain, hypoglycaemia, hepatoxicity, fracture risk, CI in heart failure due to fluid retention and cardiac failure risk, hepatic disease and type 1 DM, drug interactions with rifampicin and paclitaxel
45
How does Acarbose treat type 2 DM?
inhibits intestinal alpha glucosidases to delay absorptions and digestion or sucrose and starch and slows glucose absorption, reduces post prandial peaks
46
Benefits of acarbose?
use if all other CI, improves glycaemic control, can be used in combination
47
Risks of acarbose?
Gi disturbance, flatulance, bloating, CI in thyroid cancer, MEN2, drug interactions with orlistat and pancreatin
48
What is orlistat and how does it work?
an intestinal lipase inhibitor which reduces fat absorption for weight loss
49
What are incretins?
they increase insulin release from beta cells post eating before glucose levels become elevated 2 types: glucagon like peptide 1 (GLP1) and gastric inhibitory peptide (GIP)
50
What inactivates incretins?
dipeptydyl peptidase 4 (DPP4)
51
Why is GLP1 not as useful in diabetic treatment and what could be used instead?
has a very short half life and must be given as a continuous SC injection treatment to inhibit DPP4 which inactivates GLP1 would be more successful e.g. sitagliptin and vildagliptin
52
Benefits of DDP4-I?
can be used in combination if good glycaemic control, and good for those at risk of hypoglycaemia
53
Risks of DDP4-I?
hypersensitivity reactions so only continue if beneficial metabolic response, GI disturbance, CI in serious hypersensitivity reaction, Drug interactions with TDZs
54
How do GLP-1 mimetics treat DM?
analogue of GLP1 and is an insulin mimetic, given 2x SC/day up to 1h before meal, an alternative to insulin therapy in obese patients
55
Benefits of GLP1 mimetics?
good for those with LGV or PCV driving licences, has a good fixed dose regimen and can cause weight loss due to prolonged gastric emptying
56
Risks of GLP1 mimetics?
hypoglycaemia, GI disturbance, acute pancreatitis, weight loss, CI in thyroid cance, mEN2, drug interactions with warfarin and bexarotene
57
What are the different types of insulin therapy?
rapid acting (insulin lispro) - fast onset but short duration, so no overall control, but good for evening meal if have nocturnal hypoglycaemia short acting (soluble) - work in 30mins for 4-6h, given 15mins before meal (4x/day) or continuously if labor, emergency, surgery intermediate acting (isophane insulin) - 12-24h long acting (insulin glargine) - premixed with with retarding agents to precipitate crystals which is slowly released and last >24hr, biphasic (biphasic isophane insulin) - protamine insulins 2x/day
58
What insulin therapy is best in the young?
start on immediate acting
59
What insulin therapy is used in type 2 DM?
2x daily premixed soluble and isophane insulin
60
What causes insulin therapy dose to be adjusted?
exercise, calorie intake
61
How does insulin therapy work?
replaces insulin to form GLUT4 for glucose transport
62
Risks of insulin therapy?
weight gain, hypoglycaemia, localized lipoatrophy, hypokalaemia, CI in hypersensitivity to the ingredients and hypoglycaemia, drug interactions with repaglinide, MOI, corticosteroids, levothyroxine, thiazide diuretics
63
Complications of insulin therapy?
hypoglycaemia, lipohypertrophy, local allergic reactions, insulin resistance, weight gain
64
What is the most common cause of hypoglycemia?
form sulfonylurea treatment
65
Symptoms of hypoglycemia?
66
Causes of hypoglycemia?
exogenous drugs, pituitary insufficiency, liver failure, addison's, islet cell tumours, immune hypoglycemia, non pancreatic neoplasms
67
Diagnosis of hypoglycemia?
blood glucose
68
Treatment of hypoglycemia?
treat immediately with rapidly absorbed carbohydrate of glucogel orally or UV dextrose if unconscious, IM glycogen mobilizes hepatic glycogen, monitor levels to prevent recurrence pancreas transplant if diabetic with immunosuppression for kidney transplant, lasting graft function, pancreatic islet transplant from cadaver harvesting and injecting into portal vein
69
How is glycaemic monitoring done?
finger prick blood test with reagent strips and reading meter, 4 samples 2x/week and record urine test in those unable to do so but less reliable as urine glucose lags behind blood glucose ketostix to measure ketones if unwell to indictae serious metabolic derangement hospital detection of HbA1c is a good measurement of glucose over Hb lifespan
70
What is the aim of HbA1c in diabetic and non diabetic patients?
diabetic = 48-59mmol/mol | non diabetic = 20-42mmol/L
71
What test is useful for hypoglycemia in thalassemic patients?
glycosylated plasma proteins
72
What are insulinomas?
rare pancreatic islet cell tumours that secrete insulin and presents with fasting hypoglycemia and neuroglycopenia and SNS symptoms
73
Complications of diabetes?
hypertension, increased stroke risk, MI, diabetic foot, nephropathy, peripheral neuropathy, retinopathy, erectile dysfunction, depression, IHD, persistent and recurrent infections
74
What is the main cause of death in diabetics?
vascular disease, MI is 4x more common in DM and stroke 2x more common, women at a higher risk
75
What is macrovascular disease in DM and its treatment?
atherosclerosis, stroke, IHD, PVD - good diabetic control antihypertensives, modify risk factors, stop smoking, statins, ACEI, low dose aspirin
76
What is microvascular disease in DM?
specific to diabetes, affecting the small vessels including the retina, renal glomerulus, nerve sheath and occurs about 10-20 years after diagnosis?
77
How does nephropathy from glomerular disease present?
thickened glomerular basement membrane, diffuse of nodular glomerulosclerosis, microalbuminuria, negative protein in urine dipstick but urine ACR >3mg/mmol
78
How can nephropathy in glomerular disease develop?
progress to intermittent albuminuria and persistent proteinuria, frank nephrotic syndrome, eventually leading to end stage kidney failure
79
Treatment of nephropathy in glomerular disease?
yearly dipsticks to check protein and microalbuminuria to prevent frank proteinuria, control BP and ACE-I, dialysis and transplant
80
How does nephropathy from ischemic lesions present?
afferent and efferent arteriolar hypertrophy and hyalinisation
81
How does nephropathy with infective lesions present?
can lead to renal papillary necrosis and renal papillae can be shed in the urine and cause urethral obstruction
82
How common are eye problems in diabetics?
1/3 of young get visual problems, 5% become blind after 30 years, prevalence is falling
83
What are the different types of diabetic retinopathy?
background (30%)- microaneurysms, haemorrhages, hard exudates and can lead to maculopathy pre proliferative - cotton wool spots (microvascular infarcts), hemorrhages and venous bleeding, signs of ischemia proliferative - new vessels form due to retinal damage which can cause retinal ischemia, prolifferate, bleed, fibrose and detach from the retina maculopathy - damage to the macular and can cause macular oedema causing low acuity
84
What is diabetic retinopathy?
lesions in the retina and iris, most common cause of blindness under 65 caused by capillary endothelial change causing vascular leak, microaneurysms, capillary occlusion, local hypoxia, ischemia and new vessel formation
85
Treatment of diabetic retinopathy
annual retinal screening with visual acuity, retinal photography, aspirin, better glycaemic control, lower BP, smoking cessation
86
Treatment of maculopathy?
prompt laser, intravitreal steroids, anti angiogenic agents if macular oedema
87
What other eye problems are caused in diabetes?
cataracts, external ocular palsies (mainly 6th and 3rd), rubeosis iridis (can lead to glaucoma)
88
What is cataracts?
can be juvenile snowflakes or senile which occur earlier in diabetic patients, leading to temporary blurred vision caused reversible osmotic changes in the lens in those with hyperglycemia
89
What is diabetic neuropathy?
decreased sensation, absent ankle jerks, neruopathic deformity (pes cavus, claw toes, loss of transverse arch, rocker bottom sole), patchy sensory loss, symmetrical sensory polyneuropathy
90
What causes isolated mononeuropathies?
occlusion of the vasa nervorum
91
What causes diffuse neuropathies?
accumulation of fructose and sorbitol which disrupts the structure and function of the nerve
92
What are the different types of progressive neuropathy?
symmetrical sensory polyneuropathy (the most common form) and autonomic neuropathy
93
Symptoms of symmetrical sensory polyneuropathy?
affects the feet first, with loss of vibration, pain and temperature sensation and impaired proprioception can lead to unrecognised trauma with vlistering leading to ulceration, neuropathic arthropathy in the ankle and knee causing a deforms and swollen joint involvement of motor nerves can cause muscle wasting in the hand and a distorted foot with a hgih arch and clawing of the toes
94
Symptoms of autonomic neuropathy?
affects the CV (resting tachycardia, loss of sinus arrhythmia, postural hypotension), GI (diarrhea, gastroparesis), bladder (incomplete emptying) and erectile dysfunction
95
What are the different types of reversible neuropathy?
acute painful, mononeuropathy, mononeuritis multiplex, cranial nerve lesions, isolated peripheral nerve lesions, diabetic amyotrophy
96
Symptoms of acute painful neuropathy?
burning/ crawling pains in lower limbs, worse at night and pressure from bed clothes can be intolerable
97
Symptoms of mononeuropathy/mononeuritis multiplex?
where one of more nerves are affected, can be abrupt and painful lesions, more common at sites of external pressure, with pain, ptosis, diplopia and sparing of pupillary function
98
Symptoms of diabetic amyotrophy?
asymmetrical, painful wasting of the quadriceps, the wasting is marked and knee reflexes are diminished or absent
99
What foot damage can occur in diabetes?
ischemia and haemorrhage and tissue necrosis leading to ulceration, infections, gangrene, dcellulitis, abscess and osteomyelitis, bone deformity, absent dorsal pedis pulses
100
Prevention and treatment of feet in diabetes?
daily foot examination, comfortable shoes, no bare foot walking, regular chiropody to remove callus, relieve high pressure areas with best rest and therapeutic shoes, metatarsal head surgery, IV antibiotics for cellulitis, surgery if abscess or deep infection, good local wound care, reconstructive vascular surgery in area of arterial occlusion
101
What causes increased infections in diabetes?
impaired function of polymorphonuclear leucocytes particularly in urinary tract and skin, TB and mucocutaneous candidiasis are common, can leading to further loss of glycemic control and cause ketoacidosis
102
What effect does diabetes have on the skin?
lipohypertrophy, necrobiosis lipoidica deabeticorum (erytheatous plaques over the shins with a brown waxy discolouration), vitiligo (symmetrical white patches), granuloma annulare (flesh coloured rings and nodules over extensor surfaces of fingers)
103
How can lipohypertrophy be avoided?
varying the injection site of the insulin day to day
104
Prognosis of diabetes?
1 - good health, but increased risk of complications so must have good control, blood pressure and weight 2 - 75% die of heart disease, 15% of stroke, CV disease is 5x more common for every 1% increase in HbA1c level there is an increase in death from diabetes by 21%
105
What is diabetic ketoacidosis?
hyperglycaemia (blood glucose >11mmol/L), acidaemia (pH3mmol/L) or significant ketonuria (>2 on urine stix)
106
When does ketoacidosis occur?
in starvation states, the body can no longer metabolize carbohydrates as the body is less efficient, there is excess glucose that cannot be taken up or metabolized due to lack of insulin so the body goes into starvation state for energy production, this produce acetone, increase in hepatic gluconeogensis, peripheral lipolysis increasing free fatty acids which is converted into acidic ketones
107
What increases the effect of and triggers ketoacidosis?
stress hormones (catecholamine, glucagon, cortisol) which are secreted in response to dehydration and intercurrent illness, infection, discontinuation or inadequate insulin, CV disease, steroids, menstruation, pancreatitis, chemo
108
In who is ketoacidosis seen?
in 4% of type 1 DM, especially in newly presenting, hospital patients, rare in DM 2 unless older, overweight, non white and newly presenting
109
Presentation of ketoacidosis?
polyuria, polydipsia, vomiting, dehydration, altered mental state, coma, weight loss, anorexia, weakness, lethargy, Kussmaul respiration (deep hyperventilaton) and acetone fruity breath dry mucous membranes, dry tongue, decreased skin turgor/skin wrinkling/reduced tissue turgor, sunken eyes, slow capillary refill, tachycardia, weak pulse, hypotension
110
What will investigations show in ketoacidosis?
chest may have pneumonic consolidation, pericardial rub, murmurs, may have intra abdominal precipitant, altered mental status, abscess, boils, rashes glycosuria and ketonuria, elevated glucose levels, ketonaemia, raised WCC, high sodium due to dehydration, hyperkalaemia due to acidosis, elevated urine and creatinine due to AKI plasma osmolarity >290mOsm/kg anion gap is >13mmol/L
111
How is plasma osmolarity calculated?
2(na+k+urea+glucose)
112
How is anion gap calculated?
na-(cl+hco3)
113
DD of diabetic ketoacidosis?
alcoholic ketoacidosis, hyperosmolar hyperglycemic state, lactic acidosis, aspirin overdose, acute pancreatitis, sepsis without ketoacidosis, acute abdomen, ketoacidosis due to starvation
114
Management of diabetic ketoacidosis?
replace fluid, remove ketones, replace electrolyte loss, replace insulin, restore acid base balance, shift potassium back into cells, ABC, O2 monitor, ECG monitor, large bore peripheral IV access, urinary catheterisation to monitor urine output, LMWH and TED stockings, nasogastric tube if drowsy or vomiting, IV insulin infusion, 5% dextrose once glycemia is normal to prevent hypoglycemia, treat underlying cause, regular monitoring
115
What is classed as severe DKA?
1 of the following: blood ketones >6mmol/L bicarbonate 100 or 16
116
Who is DKA needs specialist input?
elderly, pregnant, 18-25, heart or kidney failure, serious comorbidities, fluid administration and deficits
117
Complications of DKA?
cerebral oedmea, headache, pulmonary oedema, hypoglycemia, arrhythmia, brain injury, death, hypokalaemia, metabolic acidosis, myocardial suppression, venous thromboembolism, MI, retinopathic changes, ARDS
118
Prognosis of DKA?
high mortality rate, but rates are decreasing, prognosis is worse with age and severe underlying causes, death mainly by cerebral oedema in the young and pneumonia, MI and sepsis in adults
119
Prevention of DKA?
good diabetic control, educate on risk factors and symptoms, monitoring, psychological support
120
What is a hyperosmolar hyperglycaemic state (HHS)?
marked hyperglycaemia (>40mmol/L) causing osmotic diuresis with hyper osmolality leading to an osmotic shift of water into the intravascular compartment causing severe intracellular dehydration hypovolaemia and osmolality is usually >320mOsmol/kg there is enough insulin to prevent ketogenesis but not enough to reduce blood glucose metabolic emergency and seen in type 2
121
Other causes of HHS?
MI, infection, stroke, hyperthermia, burns, GI bleed, pancreatitis, AKI, metformin, diuretics, bbs, dialysis, ccb, diabetes, poor diabetic control
122
Prevalence of HHS?
low incidence but increasing prevalence due to the increase in DM2
123
Risk factors for HHS?
DM2, elderly, nursing home residents, dementia, sedative drugs, heat waves, propensity to infection, children with long term steroid use or gastroenteritis
124
Presentation of HHS?
generalised weakness, leg cramps, visual impairment, nausea, vomiting, bed bound, confused, lethargic, reduced endogenous insulin levels, focal neurological symptoms, seizures, coma, dehydration, tacycardia, hypotension, Increased RR, Hb desaturation, hypothermia
125
DD of HHS?
lactic acidosis - when blood lactate is >5mmol/L (a rare complication of metformin)
126
Investigations of HHS?
marked glycosuria, plasma glucose >30mmol/L, serum osmolarity is >320mmol/L, AKI, cultures to test for infection, pH >7.3,
127
Management aims of HHS?
treat underlying cause, replace fluid and electrolyte loss, normalise blood glucose, prevent and assess complications
128
Initial HHS management?
ABC, resuscitation, ventilate, IV access, ECG monitor, SaO2 monitor, BP monitor, O2, catheterise, nasogastric tube, ICU, alert diabetic team, LWMH
129
Management of HHS?
calculate osmolality, fluids and electrolytes, a fall in blood glucose of 5mmol/L/hour , low dose IV insulin after, drink as soon as it is safe, fluid balance chart, replace K+ when urine flows
130
Complications of HHS?
higher mortality than DKA with vascular complications, MI, stroke, peripheral arterial thrombosis, seizures, cerebral oedmea, ischemia, infarction, DVT, PE, ARDS, DIC, multi organ fialure, rhabdomyolysos, cerebral oedema mortality is high but improved, raise awareness

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