Please enable JavaScript.
Coggle requires JavaScript to display documents.
PBL 2 Summary Steven 19 year old male (Symptoms: Polydypsea, nocturia,…
PBL 2 Summary Steven 19 year old male
**Signs:
GCS 11 semiconscious, dehydration, ketotic breath, BP 96/68, urine Glucose + Ketones, Dehydrated.
Kussmauls breathing:
- Typically with someone with acidosis.Acidic because of the ketone bodies, because using ketone bodies for energy, trying to breath off the acid. Bicarbonate buffer system: CO2 + H2O -> H2CO3 -> H+ + HCO3 reversible. If increase in H+ shifts back the other way to try release CO2 trying to get rid of increase of H+. Quickest way to get rid of acid is to breathe it off. Kidneys can excrete the H+ ions. Kidneys and lungs main organs. Can give bicarb. CO2 in his case has gone down because he has being blowing it off.
High K+
Ketotic breath
- beta oxidation making acetyl coA and ketone bodies. Acetone is the most volatile ketone causing ketotic breath. In the blood because got to get from the liver into the cells because need to use it for energy as glucose can't get into the cells.
Social
- good social support, fit and active, parental support, 19 can consent but is semi-unconsious. Whether able to consent perhaps depends on what he's consenting to. Emergency treatment to him regardless of what Mum says if not in best interest of patient.
GLUT receptors: - Glut receptors in the gut is GLUT1 in gut epithelial. Some receptors are insulin independent which is in the brain (GLUT1 and 3). GLUT4 is insulin dependent.
Investigations:
- High potassium, arterial blood gases, VBG's, BP, HR,
High Potassium in blood
- High H+ content outside the cell so H+ brought into the cell which makes the K+ want to leave the cell. This increases the K+ in the blood. (Australian College of Pathologists- will explain any blood tests)
Blood pressure
: loss fluid from intravascular space. Will also lose extracellular fluid because this will diffuse into intravascular space. HR increase to compensate high blood pressure. RR: CO2 blow off.
Symptoms: Polydypsea, nocturia, weightloss, malais
e
Hard to wake in morning
:
Malaise:
- increase in blood acidity. Increase in lactate (anaerobic). Glut 4 is insulin dependent (GLUT4 in skeletal muscles)
Weightloss
Lack of Glucose in the cells so stimulates break down of fats through lipolysis and b- oxidation for energy production. Ketogenesis in liver cells. Increased appetite due to low intracellular glucose stimulating Ghrelin.
Nocturia
- (polyuria is large volumes of urine, not necessarily frequency). He has Polyuria
Polydipsia
- osmoreceptors detect youve got more osmolality. More glucose in the kidneys being excreeted due to high glucose in the blood. This draws water with it due to high osmolality. Therefore thirsty
PPD: Support services, how you encourage, etc.
PPH: Epidemiology
- Commonalities of type 1 diabete: 2% of the population (less common). Type 2 diabetes population (50% by 2020)
Incidence
: new cases per year
Prevalence
: total cases in population at a given point in time. Aetiology: what causes it.
Type 1:
autoimmune and genetic.
Type2
: genetic and lifestyle (more genetic influence)
Cells: B cells destruction. Diabetogenic = cortisol. Alpha cells- Glucagon.
Insulin receptor- tyrosine kinase receptor then stimulates cAMP and then GLUT 4 protein