Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI, liver, kidney > Diabetes (corticosteroids/hyperkalaemia) > Flashcards

Diabetes (corticosteroids/hyperkalaemia) Flashcards

1
Q

What is fetor hepaticus?

A

Sweet smelling breath that happens in a DKA?

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

What drug protects kidney function in diabetes?

A

SGLT2 inhibitors

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

What is diabetes

A

Diabetes mellitus is anetdeficiencyofinsulinleading to imbalance in glucose production and utilization

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

Criteria for diabetes diagnosis

A
  • Characteristics of Diabetes Mellitus AND 1 of:
  • Random Blood Glucose >11.0mmol/L
  • Fasting blood Glucose >7.0 mmol/L
  • HbA1c >48mmol/mol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What genes are associated with T1DM?

A

HLA-DR3/4

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

Pathophyisiology of T1DM

A

Autoimmune complete destruction beta cells in islets of Lange than in pancreas - antibody destruction

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

Bloods to investigate T1DM?

A
  • HBA1c
  • Cpeptides
  • Islet cells
  • GADS
  • IA2
  • ABG/VBG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology of T2DM

A

Increased glucose transport ion, decreased incretin effect in gastro, impaired insulin secretion, increased glucagon secretion, increased hepatic glucose production, neurotransmitter dysfunction, decreased glucose uptake

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

Mechonism of action of SGLT2 inhbiitors

A

prevents re-absorption of glucose and sodium

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

What groups can DPP4s be used in

A

use in elderly, can be used in low eGFR,

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

GLP-1 mechanism of action

A

works on GI tract - slows digestion, feel full for longer, help lose weight. Improves insulin sensitivity, decreased lip plus is, neurotransmitter

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

Sulfonureas mechanism of action

A

target insulin secretion in beta cells, produce more insulin. Causes weight gain. Tackle steroid therapy.

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

What type of diabetes do you not treat with sulfynureas

A

T1DM
monogenic, not overweight

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

What is LADA, how does it present and how treated?

A

Latent autoimmune diabetes
Autoimmune condition slowly and progressively destroys pancreas insulin producing cells
Often present with DKA
Treat as having type 1 DM - insulin dependent

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

What conditons can cause pancreatic damage and therefore secondary diabetes?

A

Pancreatitis

Pancreatic cancer

Cystic fibrosis

Haemochromatosis

Pancreatectomy

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

What genes causes monogenic diabetes?

A

HBF-alpha
HNG4- alpha
HNF1- beta - insulin manage, predisposed to renal cysts, electrolyte imbalances (70% of cases, manage with glucozide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When does monogenic diabetes develop?

A

Below 25

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does insul,in allow in fed state

A
  • Promotes glycognesis - storage of glucose
  • inhibiting gluconeogenesis and ketogenesis - (glucose and ketone release)
  • Inhibits breakdown of current fuel storage proteolysis, lipolysis, glycogenolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is kussmarul breathing?

A

Deep and laboured breathing associated with severe metabolic acidosis - eg ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Symtptoms of diabetes

A
  • Frequent urination
  • More stressed/tired
  • Being thirstier
  • Blurred vision
  • Loss of weight
    -Slower healing time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

History qs for diabetes

A
  • Onset
  • Physical exam - Dark pigmentation in skin folds
  • Age
  • Weight loss - gradual/sudden
  • Recent environmental trigger
  • Antipsychotics
  • Family histroy
  • Prev HBA1c prev HB
  • Cute or breaks in skin that don’t heal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Risk factors for T2DM

A
  • Family history - 15% chance on parent, 75% if 2 parents
  • Ethnicity - south Asian
  • History of gestational diabetes
  • High GI diet, low fibre diet
  • PCOS
  • Central obesity
  • Metabolic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Complciations diabetes

A
  • Macrovascular - stroke/MI
  • Microvascular
  • Retinopathy
  • Nephropathy - micro alumni creatinine ratio urine
  • Gastroparesis - makes diabetes more difficult to manage
  • Sexual dysfunction
  • Quality of life
  • DKA/HHS and hypos
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment for DKA

A
  • Crystalloid fluid to restore circulating volume
  • Insulin - correct acidosis
  • Potassium
  • Glucose - allow to continue use insulin without becoming hypoglycaemic
  • Never stop basal insulin A give alongside DKA protocol and VRII
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

HSS symptoms

A
  • Frequency of urination
  • Thrust
  • Dry skin
  • Dosrientstion
  • Drowsiness and gradual LOC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

HSS parameters

A

NOT acidotic on blood gas
- Blood glucose > 20 mmol/L
- Blood ketones < 3 mmol/L
- Serum osmolarity > 320 (2(Na+K)+glucose+urea)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Symptom histroy IBD

A
  • ptom history IBD
    • Pain/discomfort
    • Bowels opening
    • Consistency
    • Blood/mucus
    • Timing noctural
    • Sensation/tenesmus
    • SOCRATES
    • Bristol stool chart
    • Melana
    • Haematochezia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the diagnositc levels of glucose on fasting and random/oral 75g glucose tolerance test?

A

Fast > or = to 7.0mmol/l
Random/oral test > or = 11.1 mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the diagnositc levels of glucose on fasting and random/oral 75g glucose tolerance test?

A

Fast > or = to 7.0mmol/l
Random/oral test > or = 11.1 mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

When do you have to do two glucose tests to confirm a diagnosis?

A

When the patient is asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What HbA1c level is diagnositc of diabetes?

A

greater than or equal to 48
a value below doesnt exclude diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What conditions mean HbA1c testing for diabetes is unreliable?

A

Conditions caused by increased red cell turnover eg
Haemoglobinopathies
Haemolytic anaemia
Untreated iron deficiency anaemia
Suspected gestational diabetes
Children
HIV
CKD
Hyperglycaemia causing meds eg corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What glucose level suggests impaired fasting glucose? (IFG)

A

Fasting glucose between 6.1 and 7.0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How is impaired glucose tolerance (IGT) defined diangostically?

A

Fasting plasma glucose < 7mmol/l
Oral glucose tolerance test - 2 hour value between 7.8 and 11.1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What levels of potassium are considered hyperkalaemia?

A

> 5.5 = hyperkalaemai
Mild – 5.5-5.9 mmol/L
Moderate – 6.0-6.4 mmol/L
Severe – >6.5 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Hyperkalaemia on ECG

A

Tall tented T waves
Loss of P waves
Broad QRS complexes
Prolonged PR interval
Sinusoidal wave pattern

AV block
Bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

When is hyperkalaemia treated?

A

> 6.5/7mmol/l and/or hyperkalaemia with ECG changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Management of hyperkalaemia

A

Calcium gluconate 10% slow IV 10-20ml
Actrapid - 10U in 50ml of 50% glucose
Consider:
Nebulised salbutamol
Correcting acidosis with HCO3- infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Aim of calcoum gluconate treatemtn in hyperkalaemia

A

Stabilise cardiac membrane
Does NOT lower serum K+ levels

39
Q

Why do yuo give insulin/dextrose infusion/ nebulised salbutamol in hyperkalaemia?

A

Shifts K+ from ECF into cells (ICF) due to cotransport with glucose

40
Q

Further management of hyperkalaemia

A

Stop offending drugs eg ACEis
Treat underlyig cause
Lowe total body potassium

41
Q

How do you lower total body K+?

A

Calcium resonium
Loop diuretics
Dialysis (AKI + persistent raised K+)

42
Q

What is IV adenosine used for?

A

Cardiac arrhytmias

43
Q

Opioid toxicity symptoms

A

Respiratory supression
Decreased GCS
Pinpoint pupils

44
Q

What should you do with corticosteroid dose when patient has intercurrent illness?

A

Double it

45
Q

Why can long term corticosteroid use precipitate an Addisonian crisis?

A

Corticosteroids supress the natural production of endogenous steroids

46
Q

Endoscrine side effects of glucor=corticoids?

A

impaired glucose regulation
increased appetite/weight gain
hirsutism
hyperlipidaemia
Cushings syndrome

47
Q

MSK side effects of glucocorticoids

A

osteoporosis
proximal myopathy
avascular necrosis of the femoral head

48
Q

Psychiatric side effects of glucocorticoids

A

insomnia
mania
depression
psychosis

49
Q

Why can glucocorticoids cause reactivation of TB?

A

Immunosuppression

50
Q

GI side effects of glucocorticoids

A

Peptic ulceration
Acute pancreatitis

51
Q

Opthalmic side effects of glucocorticoids

A

Glaucoma
Cataracts

52
Q

Side effects of mineralocortocoids

A

Fluid retention
HPTN

53
Q

Why are glucocoticoids often not used in chidlren?

A

Growth suppression

54
Q

What may precipitate infection due to glucocorticoids?

A

Imunosuppression and neutrophilia

55
Q

When is gradual withdrawak from systemic corticosteroids recommended?

A

> 40mg prednisolone daily > 1 week
3 weeks treatemnt
Recently repeated courses

56
Q

What is empagliflozin?

A

SGLT2 inhibitor

57
Q

What is the target range for diabetes control?

A

HbA1c - <48

58
Q

When should an SGLT2 inhibitor be prescribed in T2DM?

A

CVS disease risk >10% QEISK
CVS disease have
Chronic HF

59
Q

What is the maximum daily dose of metformin?

A

2g

60
Q

When should you add a second drug for diabetes control?

A

when HbA1c is over 58 mmol/mol/7.5%

61
Q

Diet advice diabetes

A

High fibre, low glycaemic index
Low fat dairy and oily fish
Limit sat fat and sucrose
target weight loss 5-10%

62
Q

How often should HbA1c be checked in T2DM>

A

3-6 months until stable then 6 monthly

63
Q

2nd line if metformin not tolerated

A

(try modified release first if can)
DPP4 inhibitor or pioglitazone or sulfonylurea IF not at risk of CVD/ no HF
Otherwise SGLT2

64
Q

Why is metformin titrated up slowly

A

Avoid GI upset

65
Q

3rd line therapy

A

Add another drug from 2nd line OR
Insulin based treatemnt

66
Q

WHen Switch to GLP-1 mimetic in T2D,?

A

if BMI >35kg or
insulin would have occupational complications
when triple therapy is not effective or tolerated
Switch one of drugs for GLT 1 mimetic
Specialist med

67
Q

What insulin start with if need in T2DM?

A

Human NPH insulin - isophane, intermediate acting at bed/ 2x a day

68
Q

What is cpeptide blood test testing for
Parameters and when require

A
  • how well function pancreas is with a random glucose.
    Early is fine
    under 0.3 = T1DM, under 0.6 requires insulin
69
Q

WHy do you give potassium with IV dextrose in DKA?

A

allow to continue to use insulin without → hypokalaemIa or hypoglycaemia - gradual return to normal

70
Q

Environmental triggers for T1DM

A

viral, bereavement, toxin, drug or chemical - if have autoimmune genes for type I

71
Q

Why do annual eye test and retinal test in diabetes?

A

Microvascular damage to eyes and kidneys

72
Q

Why need Hb level to determine if HbA1c is accurate

A

glycosylation of blood cells - if don’t have HB in range not accurate HBA1c

73
Q

Why ask about history of antipsychotics in diabetes?

A

Risk factors

74
Q

What is DKA?

A

Complex disordered state characterised by hyperglycaemia, acidosis and ketonaemia

75
Q

Range for tests in DKA - ketones, bicard, blood glucose, VBG

A
  • Blood ketones > 3 mol/L (normal under 0.3)
    • Capillary ketones more accurate than urinary
  • Bicarbonate < 15 mmol/L and/or pH <7.3
  • Blood glucose > 11 mmol/L
  • Venous blood gas in ketonaemia, rule out acidemiA
76
Q

Levels of glucose, ketones and osmolarity in HSS

A
  • Blood glucose > 20 mmol/L
  • Blood ketones < 3 mmol/L
  • Serum osmolarity > 320 (2(Na+K)+glucose+urea)
77
Q

Why caustionin fluid replacement in HSS?

A

Risk of cerebral oedema

78
Q

Is blood gas acidotic in HSS?

A

No

79
Q

What exam is important in diabetes?

A

Foot exam - pulse, sensation, skin integrity
Peripheral neuro[athy risk

80
Q

Signs of DKA

A

Tachycardia
Hypotension
Reduced skin turgor
Dry mucous membranes
Reduced urine output
Altered consciousness (e.g. confusion, coma)
Kussmaul breathing

81
Q

What would an ABG show in DKA?

A

PaO2: may be reduced in the context of pneumonia (e.g. DKA precipitated by a respiratory infection).
PaCO2: may be low in the context of DKA due to respiratory compensation as a result of metabolic acidosis.
pH: low in the context of DKA due to the presence of acidic ketones.
HCO3-: low in the context of DKA due to metabolic acidosis.

82
Q

rISK FACTORS FOr T1DM triggering

A

diet, vitamin D exposure, obesity, early-life exposure to viruses associated with islet inflammation (such as enteroviruses), and decreased gut-microbiome diversity.

83
Q

What other diseases are people with T1DM at risk of?

A

Other autoimmune diseases
Graves disease, Hashimotos thyroiditis, autoimmune gastritis and/or perniciious anaemia, coeliac disease, vitiligo, addisons disease

84
Q

When to suspect T1DM in an adult

A

Ketosis.
Rapid weight loss.
Age of onset younger than 50 years.
Body mass index (BMI) below 25 kg/m2.
Personal and/or family history of autoimmune disease.

85
Q

When to suspect T1DM in a child

A

Polyuria.
Polydipsia.
Weight loss.
Excessive tiredness.

86
Q

How does mild hypoglycaemia present?

A

Hunger.
Anxiety or irritability.
Sweating.
Tingling lips.
Irritability.
Palpitations.
Tremor.

87
Q

How does severe hypoglycaemia present?

A

Weakness and lethargy.
Impaired vision.
Incoordination.
Reduced orientation.
Confusion.
Irrational behaviour.
Emotional lability.
Deterioration of cognitive function (when blood glucose levels fall lower than 3.0 mmol/L).

88
Q

COMplications of severe hypoglycaemia

A

Convulsions.
Inability to swallow.
Loss of consciousness.
Coma.

89
Q

Insulin manangement in most T1DMS

A

Basal bolus regimine
Basrline longer acting insulin
Bolus short acting insulin for meals and snakcs

90
Q

What is acanthosis nigricans?

A

Skin condtions causng dark pigmentation of ksin folds suggesting insulin resistance

91
Q

What drugs increase risk of T2DM?

A

Statins, corticosteroids, and combined treatment with a thiazide diuretic plus a beta-blocker

92
Q

wHAT conditions increase risk of T2DM

A

PCOS
metabolic eg fatty liver disease, BP high etc

93
Q

What is it important to monitor with metformin?

A

Renal function
B12 levels - risk of low as higher metformin dose

94
Q

What is a pioglitazone?

A

Diabetes drug that can be used with metformin, sulfonylurea or insulin.
Thiazolidinediones
Increases sensitivity to insulin

GI, liver, kidney (50 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions