Endocrine Core Conditions Flashcards

(39 cards)

1
Q

What is diabetic ketoacidosis?

A

Acute metabolic complication of diabetes (type 1) which is potentially fatal

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2
Q

How is DKA characterised?

A

Absolute insulin deficiency (hyperglycaemia)
Ketonuria
Acidosis

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3
Q

What is DKA the most common complication of?

A

Acute hyperglycaemic complication of diabetes

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4
Q

What are the causes of DKA?

A

Inadequate insulin therapy
Infection (release of epinephrine which releases glucagon- inc blood glucose levels & need for alternative energy-ketones)
MI/stroke
Drugs: Steroids, 2nd gen antipsychotics, thiazides

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5
Q

What are the signs & symptoms of DKA?

A
Polyuria
Polyphagia
Polydipsia
N&V
Weakness
Weight loss
Kussmaul breathing
Acetone (pear drop breath)
Sunken eyes
Altered consciousness/ mental status
Acute cerebral oedema
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6
Q

What is the pathophysiology of DKA?

A

1) Reduction in net circulating insulin
2) Causes elevation of counter hormones (Glucagon, cortisol, growth hormone)
3) Lead to inc gluconeogenesis, hepatic & renal glucose production & impaired glucose utilisation in peripheral tissues
4) Hyperglycaemia & hyperosmolarity
5) Insulin deficiency leads to release of FFA from adipose tissue, hepatic fatty acid oxidation, formation of ketone bodies
6) Ketonaemia & acidosis

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7
Q

How are ketone bodies formed?

A

Lipolysis (fat broken down into free fatty acids)
FFA sent to the liver where they are turned into ketone bodies
-Acetoacetic acid
- Beta hydroxybutyric acid

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8
Q

What are the pro’s and con’s of ketones?

A

Pro’s: Can be used for the body for energy
Con’s: Make the blood more acidic (Kussmaul respiration), more K+ in the blood (hyperK) but reduced stores, high anion gap

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9
Q

What is the mechanism of Kussmaul breathing?

A

Deep laboured breathing

Body tries to reduce CO2 intake and therefore the acidity of the blood

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10
Q

What is the treatment of acute DKA?

A
IV fluids: Isotonic saline (0.9% NaCl)
When p.glucose 11.1 change to 5% dextrose w/0.45% NaCl
Consider ICU
IV insulin (FRIII)
IV Potassium Phosphate when K+ <3.5
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11
Q

In DKA what are the indications for ICU admission?

A
Haemodynamically unstable (AKI)
Cariogenic shock (HF)
Altered mental status
Pregnant
Oliguria/anuria
Sats <92% room air/ <90s after 2L fluid
Respiratory insufficiency
HCO3 <10
Severe acidosis <7.1
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12
Q

How is acute DKA differentiated from mild/moderate DKA?

A

Absence of:
Orthostatic/supine hypoT
Dry mucous membranes
Poor skin turgor

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13
Q

How is mild/moderate DKA treated?

A

IV fluids: Isotonic saline >1hour add potassium phosphate if levels <3.5
Insulin when K+ >3.5

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14
Q

How is DKA investigated?

A

3 features for diagnosis:

  • Plasma glucose: >11mmol OR known DM1
  • ABG: pH <7.3, bicarb <10s >15m
  • Urinalysis: Glucose & Ketones ++ OR blood ketones >3

Other: Bloods: U&E, lactate, anion gap, electrolytes

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15
Q

What is severe DKA characterised by?

A
Blood ketones >6
Bicarb <5
pH <7
HypoK <3.5
GCS <12
O2 <92% on room air
sBP <90
HR >100, <60
Anion gap >16
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16
Q

What definition is given when DKA is resolved?

A

Blood ketones <0.6mmol/L

Venous pH >7.3

17
Q

How often should obs be done on a patient with DKA?

A

Sugars, Potassium, Bicarb every 2 hours for first 6 hours

18
Q

Define HHS

A

Hyperglycaemic hyperosmolar state

Inc plasma osmolarity due to extreme dehydration and increase blood concentration

19
Q

What is HHS a complication of?

A

Diabetes type 2

20
Q

What are the causes of HHS?

A
Infection
CVA/MI
Trauma
Non-compliance to medication
Drugs (Thiazides, steroids, beta blockers)
21
Q

What are the signs & symptoms of HHS?

A
Altered mental state
Polyuria &amp; polydipsia
Weight loss
Poor skin turgor (dehydration)
Dry mucous membranes
Mental status alterations
22
Q

What is the pathophysiology of HHS?

A

1) Glucose is a polar molecule so cannot passively diffuse across cell membranes
2) Glucose acts as a solute
3) High levels of glucose in the blood (hyperosmolar state)
4) Water diffuses from cells into blood vessels
5) Leads to total body dehydration

23
Q

What characteristics differentiate HHS from other diabetic complications?

A

Hypovolaemia
Hyperglycaemia >30mmol/L
Osmolality >320
NO acidosis/ketones

24
Q

How is HHS treated?

A

Fluids: IV 0.9% NaCl
vasopressors: 0.5-3micro IV NorA
Potassium
Insulin

25
How is hyponatraemia defined?
Serum conc <135mmol/L | Most common electrolyte disorder
26
What are the causes of hypoN?
HypoV: Vol depletion, third spacing Euvolaemic: SIADH, hypothyroid, adrenal insufficiency, meds HyperV: Effective decreased arterial vol (cHF, cirrhosis, nephrotic syndrome), Vol overload
27
What are the signs & symptoms of hyponatraemia?
``` Headache Confusion Balance difficulties Acute cerebral (coma, vomiting, altered mental state, seizures) Pulmonary oedema Low urine output Orthostatic hypotension Abnormal JVP ```
28
How is hyponatraemia managed?
``` Acute: Hypertonic 3% saline infusion Treat underlying HypoV: Isotonic IV 0.9% saline HyperV: Fluid restriction 1L/day, adjunct: Furosemide ```
29
What is Na homeostasis controlled by?
``` ADH from posterior pituitary Kidneys Aldosterone Vasopressin Thirst ```
30
What is the pathophysiology of Na retention/excretion?
1) Drink water 2) Blood diluted= dec plasma osmolality 3) Hypothalamus signals pituitary to dec ADH secretion 4) Fewer aquaporins opened in distal convoluted tubule 5) Dilute urine & Na excreted
31
What is the pathophysiology of SIADH & hypoNatraemia?
1) Body continues to excrete ADH when dec plasma osmolality 2) Dilute blood = dilute Na 3) Causing dec aldosterone production 4) More Na excreted by the kidneys 5) Water follows Na excretion by diffusion 6) Normalises fluid vol but dec Na vol
32
Define hyperkalaemia
Serum conc >6.0mmol/L
33
What are the causes of hyperkalaemia?
``` High K+ intake Dec k+ excretion Renal failure Drugs: ACEi, Spironolactone, amiloride, beta blockers Inc cell turnover/lysis Infection Severe burns, rhabdomyolysis Insulin deficiency Metabolic acidosis ```
34
What are the signs & symptoms of hyperkalaemia?
Asymptomatic Muscle weakness or flaccid paralysis Life-threatening arrhythmia (VT)
35
What changes can be seen on an ECG due to hyperkalaemia?
``` Prolonged PR interval Tall tented T waves Loss of P waves Widened QRS complexes Sine waves Arrhythmias: VF, VT, PEA Bradycardia ```
36
What is the management of hyperkalaemia?
``` 10mls Ca gluconate 10% IV over 3mins 5-10u of Actrapid in 50mls 20% Dextrose Nebulised Salbutamol 5mg IV Na2CO3 IV Furosemide Dialysis ```
37
Causes of hypoglycaemia in non-diabetics?
EXPLAINS H: Endogenous: Drugs, beta blocker/valproate/salicylate OD, OH- Pituitary insufficiency Liver disease Addison's disease Islet cell tumours, immune, infection (sepsis, malaria) Non pancreatic neoplasm: Fibroma, sarcoma, mesothelioma Starvation & malnutrition Hypothyroidism
38
What are the causes of hypercalcaemia?
Malignancy Drugs Hyperparathyroidism Sarcoidosis
39
What are the ECG signs of hypercalcaemia?
Short QT Prolonged QRS Flat T waves