Intermediate Theory Flashcards
What are some risk factors to CKD
- Diabetes
- HTN
- Obesity
- Heart problems/stroke
- Smoker
- 60+
- Aboriginal/Torres Strait
- Hx of Kidney injury
- Family hx
What are the 3 main causes of CKD?
- Hypertension
- Glomerularnephritis
- Diabetes
What symptoms may you see if a patient missed dialysis
- Hyperkalaemia and other metabolic disorders
What are the 4 kidney functions and a brief description for each
Filtration:
- passive process where fluid and solutes move across the glomerular membrane resulting in creation of filtrate.
Reabsorption:
- passive and active process whereby fluid, plasma and electrolytes are reabsorbed via the nephron into systemic circulation
Secretion:
-selective process whereby toxins and unwanted byproducts are secreted into urine
Excretion:
- excretion of waste products and excess water into ureters and excreted as urine
4 phases of Capnography
A-B = inspiratory baseline
B-C= expiratory upstroke
C-D= expiratory plateau
D = Capnog Reading
D-E = Inspiratory downstroke
What does a shark fin capnography usually indicate?
- COPD
- Asthma
IV Cannulation contraindications
- Directly over or distal to:
- burns
- infection
- cellulitis
- injury
- Frail or immunocompromised pts unless clinically uwarranted
- more than 2 attempts my by appropriately trained/skilled clinicial
- more than 1 attempt of vascular access in traumatic cardiac arrest
Supraglottic airway indications
- to manage/maintain a compromised airway in the pt w/absent pharyngeal and laryngeal reflexes
SGA contraindications
- Intact gag reflex
Direct laryngoscopy and magill forceps contraindications
- conscious patient/intact gag reflex
- do not use magills if obstructions below vocal cords
- spo2 reading of 90% and ventilation is achievable
- suspected epiglottitis
IO access contraindications
- fractured targeted bone
- IO within last 48hrs in targeted bone
- inability to locate landmarks or excessive tissue
- prosthetic limb or joint (near insertion point)
- directly over, or distal to burns, cellulitis, infection or injury.
External Jugular Access contraindicatins
- access is available by other means (PIVC/IO)
- Patients in spinal precaution
- > 1 attempt by appropriately trained and skilled clinician
- Directly over or distal to
- burns
- cellulitis
- infection
- injury
Explain the influence diabetes has on CKD. (Pathophys)
- Increase BSL combined w/lipids+proteins = inflammatory response of endothelial cells.
- Arteriosclerosis of efferent arteriole
- decrease perfusion to nephron = nephron ischemia
- backwards pressure (barotrauma) into glomerulus = increase GFR
- damage + expansion of mesingeal cells
- leads to cytokine secretion, fibrosis, then glomerularsclerosis = decrease GFR
- damage to GBR + podocytes allowing larger molecules to pass through (increase glomerulus permeability) albumin passing (glycosuria)
- JGA detects decrease in GFR - secretes renin activating RASS = vasoconstriction - worsening HTN + barotrauma
- decrease GFR progress towards CKD
= Electrolyte imbalance, metabolic acidosis, metabolic arrangement.
T1DM pathophys (approx 7 points)
- born with genetic predisposition to T1DM
- autoimmune response results in T-cell mediated destruction of insulin secreting beta cells on islets of langerhaans within pancreas.
- Beta cell production eventually leads to a complete insulin deficiency
- at 80-90% deficiency T1DM diagnosed
- causing altered pancreas function, causing excess glucagon production
-exacerbating metabolic defects.
Explain the T2DM pathophys
2 issues at play:
Insulin resistance:
- decreased amount of insulin receptors and decreased response to insulin in cells
- glucose unable to move into target cell, therefore remaining in bloodstream increasing hyperglycaemia
- persistent hyperglycaemia stimulates further secretion of insulin from beta cells
Beta cell destruction:
- continued hyperglycaemia causes beta cells to decrease in size and amount
- insulin deficiency caused by lack of beta cells
- therefore glucose also unable to move into target cells
- maintaining hyperglycaemia
State the differences between DKA AND HHS
DKA:
- T1DM
- complete deficiency of insulin results in lypolysis
- ketones released
- kussmaul breaths
- acidosis
- faster to diagnose
HHS:
- T2DM
- blood pH usually normal
- nil lypolysis due to small amount of insulin
- severe dehydration
- nil ketones
- slow progression/diagnosis
Normal function when body becomes hyperglycaemic
- Stimulant of HYPERGLYCAEMIA
- causes beta cells in pancreas to release insulin
- insulin causes glucose to be stored in liver via glycogenesis
- or it is used up by cells for energy
- causing decrease in BGL
When would you discontinue with a supraglottic airway?
- effective ventilation (adequate rise/fall) cannot be achieved (air leakage can be expected)
- GCS of the patient increases with return of gag reflex or patient attempts to remove
- I-Gel is faulty
- Regurgitation occurs and is anticipated to be compromised
What are the Indications for direct laryngoscopy and magills forceps
- to identify and remove a suspected foreign body from the hypopharynx thats prevetning ventilation
- In order to create a patent airway and an ability to achieve adequate ventilation
What are the Indications for IO access
Cannulation of the intraosseous space using EZ-IO:
Cardiac Arrest
- 1st line for paediatrics
- consideration for first line in traumatic arrest
- 2nd line cardiac arrest management for adults following at least one failed IV access attempt, unless unable to locate appropriate site for IV access
All other circumstances:
- where immediate meds/fluid administration is required following at least one failed IV attempt when unable to administer by any other appropriate route
What are the indications for External Jugular Access?
- Administration of IV medications/fluid where peripherally inserted IV catheters or IO catheters are inappropriate, unsuitable or unavailable
What are the contraindications of External Jugular Access?
- access is available by other means (IV/IO)
- patients in spinal precautions
- > 1 attempt by appropriately trained/skilled clinician
- directly over or distal to: burns, cellulitis, injury and infection
What are the indications for IV cannulation
- administration of IV fluids where oral intake is unavailable or unsutable
- administration of IV meds where other routes are unavailable or unsuitable
- unstable or deteriorating patients
what is the gradual process behind a STEMI?
Atherosclerosis:
1. Modifiable risk factors e.g. HTN smoking cause damage to epithelial cells that line lumen
2. LDL’s and free radicals oxidise in the tunica intima causing an inflammatory response
3. Macrophages are formed consuming LDL’s (phagocytosis) causing release of cytokines/inflammatory mediators
4. Macrophages turn into foam cells, full of LDL’s which clump together between tunica intima/media.
5. Foam cells die releasing LDL’s, forming atherosclerotic plaque and develops fibrous cap
6. Continuous damage by risk factors cause plaque instability and increase chance of rupture
7. plaque eventually ruptures causing platelet adhesion and coagulation cascade begins
8. platelet adhesion and turbulent flow increase platelet aggregation resulting in occlusion
9. thrombus formed may partially occlude vessel = angina/NSTEMI
10. In this case a full occlusion causes ischemia/necrosis resulting in Myocardial Infarction.
