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Semester 1 > Thirst > Flashcards

Thirst Flashcards

1
Q

3 processes kidney uses to conserve bicarbonate levels

A

Secretion of H+
Reabsorption if filtered HCO3-
Production of new HCO3-

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2
Q

Normal levels of pH, H, PCO2 and HCO3-

A

7.4;40;40;24

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3
Q

What happens in respiratory acidosis

A

Co2 retention drives equilibrium to the right
Therefore both h and HCO3- conc increase
The increased h conc results in acidosis
pH<7.35 and pco2>45mmHg

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4
Q

What happens in respiratory alkalosis

A

Excessive co2 removal drives equilibrium to the left
Both H and HCO3- conc fall
The decreased h conc results in alkalosis
pH>7.45 and pco2<35mmHg

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5
Q

Metabolic acidosis

A

HCO3 depleted
First priority: compensation - return pH regardless of HCO3 and pco2 conc
Second priority - correction - HCO3 and pco2

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6
Q

What happens in metabolic alkalosis

A

Loss of h+ or addition of base, causes HCO3- conc to rise

Ph>7.45 and HCO3 conc is high

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7
Q

What are fed and fasted state?

A 
1. Fed state 
Shortly after a meal, when new nutrients are available 
Metabolism in anabolic 
2. Fasted state
Body needs to draw upon its fuel stores 
Metabolism is catabolic
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8
Q

Key hormones involved in regulating metabolism

A

Insulin
Glucagon
Adrenaline and noradrenaline

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9
Q

Which hormone drives the fed state, how is it secreted and what does it do?

A

Insulin secreted by b-cells in response to elevated levels of blood glucose and the parasympathetic nervous system

  1. Stimulates glycogen synthesis in liver and muscles
  2. Stimulates uptake of glucose into muscles and adipose tissue
  3. Stimulates glycolysis and hence fatty acid synthesis
  4. Stimulates triglycerides formation in fat tissue
  5. Stimulates protein synthesis in muscle
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10
Q

Which hormone drives the fasting state, how is it secreted and what does it do?

A

Glucagon secreted from alpha cells in the pancreas when glucose conc is low

main target is liver, where it:

  1. Stimulates release of glucose from glycogen
  2. Stimulates gluconeogenesis but inhibits glucose incorporation into glycogen
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11
Q

Where are adrenaline and noradrenaline secreted from and what do they do?

A

Secreted by adrenal medulla and neurones of the sympathetic nervous system when blood glucose falls

  • Drive breakdown of glycogen and triglycerides
  • glycogenolytic action mainly on muscle
  • decrease glucose uptake by muscle so fatty acids are used as fuel
  • Increase glucagon secretion and inhibit insulin secretion
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12
Q

What is type 1 diabetes?

A

Insulin dependent
Autoimmune condition in which beta cells of pancreas are destroyed
Therefore little insulin can be secreted in response to increase in blood glucose conc
Treated by injecting insulin when required

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13
Q

What is type 2 diabetes?

A

Late age of onset
Normally less severe than type 1
Tissues are insensitive to the effects of insulin

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14
Q

What are the three elements that maintain the acid-base balance?

A
  1. buffering
  2. lungs
  3. kidneys
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15
Q

what is the equation for pH?

A

pH is proportional to bicarbonate ion concentration divided by partial pressure of carbon dioxide

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16
Q

How is acid base balance regulated?

A

Return to homeostasis via:

  1. compensation: first priority, restore pH ASAP irrespective of [HCO3-] and PCO2
  2. correction: second priority, restore [HCO3-] and PCO2

Reduction of free [H+] in solution by:

  1. chemical buffers
  2. ventilation changes (PCO2)
  3. renal system changes
17
Q

Why are patients with diabetic ketoacidosis thirsty?

A

Defect in insulin secretion leads to
• Glucose not metabolised
• Fats metabolised as fuel and form ketoacids
• Blood becomes acidotic
• Kidneys eliminate ketoacids in urine
• High glucose conc in ECF dehydrates ICF via osmosis
• High glucose conc in urine causes osmotic diuresis (i.e., glucose in tubules causes reduction in resorption of fluid –> high vol dilute urine

18
Q

What does the breakdown of fats result in?

A
  • breakdown of fatty acids leads to the formation of ketone bodies
  • this is because acetyl-CoA formed in lipolysis cannot enter the citric acid cycle
  • therefore the acetyl-coA is converted to ketone bodies
19
Q

metformin functions

A
  • increasing insulin sensitivity
  • Acts to reduce gluconeogenesis in the liver,
  • Increases glucose uptake and utilisation in skeletal muscle
  • Slightly delays carbohydrate absorption in the gut.
  • Increases fatty acid oxidation - reducing circulating LDL and VLDL
20
Q

Metformin mechanism of action

A
  • It acts on the mitochondria to change the ratio of AMP to ATP
  • ↑ AMP:ATP ratios activate AMP-activated protein kinase
  • Inhibits glucagon signaling and gluconeogenic pathways
  • AMPK increases transcription of genes important for glucose transport fatty oxidatin and inhibits fatty acid synthesis
21
Q

what are Incretins

A
  • Glucagon-like peptide-1 (GLP-1) is secreted by L-cells in the gut
  • Gastric inhibitory peptide (GIP) secreted by K-cells in gut
  • stimulate insulin biosynthesis/ secretion, inhibit glucagon secretion in pancreas, delay gastric emptying, increase cardiac output and increase brain satiety signals.
22
Q

What are sulphonylureas?

A
  • older class of orally-active hypoglycemic drugs.
  • interfere with beta cell ion channels to potentiate insulin secretion.
  • Well tolerated but can lead to weight gain by stimulating appetite.
23
Q

What are gliptins?

A
  • Enhance endogenous incretin effects by blocking DPP-4

- Lowers blood glucose by increasing first phase of insulin response after meals.

24
Q

Major predictors of poor patient adherence to treatment and medication

A

Presence of psychological problems, particularly depression

Presence of cognitive impairment

Treatment of asymptomatic disease

Inadequate follow-up or discharge planning

Side effects of medication

Patient’s lack of belief in benefit of treatment

Patient’s lack of insight into the illness

Poor provider–patient relationship

Presence of barriers to care or medications

Missed appointments

Complexity of treatment

Cost of medication, co-payment, or both

25
Q

What are the two categories of treatment beliefs?

A

necessity
- personal need for treatment

concerns
- about negative effects of treatment

26
Q

Type 1 diabetes pathophysiology

A
  • autoimmune disease
  • beta cell destruction:
    1. symptoms when 80% b cell mass lost
    2. environmental factors e.g. viral infection
27
Q

Pathophysiology of type 2 diabetes

A

Genetic factors

  • defect of b cell
  • insulin resistance

environmental factors

  • obesity
  • stress
  • reduced physical activity
28
Q

Diabetes drugs

A
  • sulphonylureas
  • biguanides (metformin)
  • a-glucosidase inhibitors
  • thiazolidinediones
  • GLPI Agonists
  • DPP IV inhibitors
  • SGLT2 inhibitors
  • insulin
29
Q

Complications of diabetes

A

Acute

  • Diabetic Ketoacidosis
  • Hypoglycaemia
  • Other emergencies

Chronic

  • Microvascular: Eyes, Kidneys, Nerves (Feet)
  • Macrovascular: Heart, Brain, (Feet)
30
Q

What are the clinical features of diabetic ketoacidosis

A

Hyperglycaemia:

  • dehydration
  • tachycardia
  • hypotension
  • clouding of consciousness

Acidosis:

  • air hunger
  • acetone on breath
  • abdominal pain
  • vomiting
31
Q

Treatments for diabetic ketoacidoses?

A

Hyperglycaemia: IV insulin

Dehydration: saline, dextrose 5% subsequently

Potassium losses: monitor K+, replace as required

32
Q

MOA of major antibiotics

A

PENICILLINS + CEPHALOSPORINS:
cell wall

AMINOGLYCOSIDES:
inhibition of polypeptide synthesis

TETRACYCLINS + MACROLIDES:
protein synthesis inhibitors

FLUOROQUINOLONES: inhibit bacterial replication (something to do with DNA gyrase?)

Semester 1 (13 decks)

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