Diabetes Flashcards

1
Q

osmotic diuresis

A

excessive production of urine

when sugar high, leaks into urine so pulls water out of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

thrush

A

white cheesy discharge
candida likes sugar in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

serum sodium level in diabetes

A

higher blood sugar, lower serum sodium

blood becomes osmolar (more solute)
osmolality sucks water out of cells
=hyperosmolar hypernatraemia (high sodium conc)

shrinks cells
dilutes the sodium
cells shrunk too much -> drowsy and unconcious
-> hyperosmolar hyperglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why might diabetic patients lose weight

A

deficient in insulin
(insulin signals that the body has glucose)
w/o insulin, body becomes catabolic and starts breaking down tissues to make sugar
breaks proteins to sugar
fat into ketones
muscle cells to amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ketones
capillary beta-hydroxybutyrate
acetoacetate

A

ketones acidic
B hydroxybutyrate is capillary ketone (more accurate measurement)

acetoacetate is urine ketone

causes acidosis in dka

above 3mmol/L is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

HCO3 measurement

A

bicarbonate
low signals metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

low PaCO2 result

A

partial pressure co2

patient hyperventilating
respiratory compensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

diabetic ketoacidosis

A

caused by insulin deficiency
precipitated by infection, steroids, trauma, hyperthyroidism

ketogenesis causes metabolic acidosis
hyperglycaemia causes osmotic diuresis and dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

biochemistry of dka

A

insufficient/no insulin
increased glucagon
breaks fat cell to glycerol and fatty acid by lipolysis
fatty acids converted to ketones

glucagon activates release of glycogen stores
stimulates release of sugar from liver

reduced uptake of glucose

muscle - amino acids,
glycerol and other subtrates in liver converted to glucose

blocked krebs cycle

increased ketone and glucose production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

treating dka

A

initially
IV drip
add insulin and saline
add na water and k

crystalloids to replace Na and K

then
subcutaneous insulin once K down (K is high at first because acidosis causes k to leak out of cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pregnancy and ketones

A

increased ketones
inc risk of ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

type 1

A

autoimmune process against pancreatic beta islet cells

inc risk of other autoimmune diseases

absolute insulin deficiency

weight loss
young people

treat w insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

closed loop system for type 1
and current

A

continuous glucose sensor

insulin pump hosting control algorithm

in development

currently
insulin 4x a time
hybrid closed loop system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

type 3c

A

damage to pancreas from exocrine pancreatic damage (alcoholic pancreatitis or pancreatic cancer)

absolute insulin deficiency

associated exocrine pancreatic dysfunction

steatorrhoea (excessive excretion of fat)
cant digest fat

treat w insulin
creon enzyme supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

type 2

A

insensitivity/ insulin resistance
defect in signalling pathway
or beta cell failure

obesity- fat not stored in fat cells, stored in muscle and liver, muscle less sensitive

less ketone prone
dka for severe cases
for BAME subjects

body produces more insulin to compensate
pancreas overworked
insulin levels drop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pathophysiology of type 2

A

beta cells produce less insulin
insulin deficiency
increased production
alpha cell produces excess glucagon
excess glucose output
hyperglycaemia

insulin resistance
decreased glucose uptake
sugar from meals not stored in muscles and fat
stays in blood stream
hyperglycaemia

17
Q

type 2 diabetes timeline

A

progressive decline in beta cell function

screening for pre diabetes before 50% can prevent

18
Q

HBA1c

A

glycated haemoglobin
shows glucose levels for past 3 months
(life span of red blood cell)
(like average glucose level)

higher means more risk of diabetic complications

19
Q

diagnosing type 1

A

autoantibodies against pancreatic islets
markers for autoimmune disease

eg
antiGAD, anti Zn transporter, anti insulinoma

20
Q

measuring c peptide

A

measures amount of endogenous insulin production

proinsulin = insulin + c peptide

cpeptide only produced by pancreas

distinguishes between insulin from patient and insulin from injection

21
Q

diagnosing type 2

A

c peptide high

low for type 1 after 6 months
low for type 3c

22
Q

diagnosing type 3c

A

CT pancreas
for chronic pancreatitis

faecal elastase levels low if exocrine deficiency

23
Q

diabetes microvascular complications

A

diabetic retinopathy
periodontal disease
diabetic nephropathy
erectile dysfunction
diabetic neuropathy

24
Q

diabetic macrovascular complications

A

stroke
depression
heart disease
fatty liver disease
peripheral vascular disease
amputation due to gangrene, infections

inc risk of atheroma and thrombus

25
Q

controlling hyperglycaemia in type 2

A

insulin sensitisation drugs

glucose excretion

insulin secretion

insulin replacement

26
Q

kussmaul breathing

A

an abnormal breathing pattern characterized by rapid, deep breathing at a consistent pace. It’s a sign of a medical emergency — usually diabetes-related ketoacidosis (DKA), which can affect people with diabetes and people with undiagnosed Type 1 diabetes