Exam

Question 1

• Pathophysiology of Type 1 diabetes

Answer 1

o Destruction of islet cells in the pancreases>
little to no insulin produced >
no insulin to bind to insulin receptor> hyperglycemia.

genetic susceptibility, autoimmunity and environmental factors, Non-autoimmune- secondary to other disease such as pancreatitis.

Question 2

• Pathophysiology of Type 2 diabetes.

Answer 2

o Insulin secretion is increased to compensate for insulin resistance in peripheral tissues> insulin fatigue of pancreases beta cells> no longer able to produce insulin> beta cells undergo apoptosis> little to no insulin production> hyperglycemia.

Question 3

Pathophysiology of acute complications of Type 1

Answer 3

Little to no insulin production metabolism of fat stores,
Acidic ketones released through ketogenesis in the liver, body tried to compensate and the breath sme;ls fruity and sweet and ketones and glucose will be present in the urine.

Question 4

Nursing management of acute complications of Type 1

Answer 4

I would order a BGL and urinalysis.
o Check baselineserum potassium levels as fluid shift can occure when iv fluid is initiated.
o ABG to check PH and if the body is compensating.
o Iv Fluids
o Fast acting inslin delivered slowly to bring down BGL.

Question 5

Pathophysiology of chronic complications of Type 2 diabetes.

Answer 5

Decrease in insulin production> high levels of serum glucose (30mmol/L)> increased osmolarity of blood due to glucose and low water> intracellular fluid moves into the intravascular fluid > severe dehydration.
 Large amount of glucose in urine (glycosuria) > water drawn together (polyuria > lead to hypovolemia and hypotension.

Question 6

Nursing managment of HHS

Answer 6

Aggressive fluid and electrolyte resuscitation
Strict control of serum glucose levels (insulin).

Question 7

Macrovascular complications of T2D

Answer 7

 Diabetic macular oedema: blood vessels leak their contents into the macular region (leading cause of decreased vision in diabetes)

 Kidneys: Hyperglycaemia > cause inflammation in the capillaries > microvascular destruction. Diabetic nephropathy.

 Diabetic kidney disease: a progressive disease caused by damage to the capillaries in the glomeruli of the nephrons

Question 8

Microvascular complications of Type 2 diabetus

Answer 8

 Vision> Hyperglycaemia > cause inflammation in the capillaries > microvascular destruction> Diabetic retinopathy: changes to the retinal blood vessels > haemorrhage or leak fluid.

 Hyperglycaemia > pro-inflammatory state> arterial endothelial damage> Initiates atherosclerosis. Embolism occurs >Lodges into coronary artery/cerebral artery > can lead to MI/Stroke.

Question 9

Neuropathic complications of T2DM

Answer 9

 Glucose attaches to neurons and changes their structure and function.
 Common symptoms of peripheral neuropathy:
 Numbness, tingling and decreased sensation
 Poor wound healing- vascular changes> Decreases the supply of white blood cells and oxygen (hypoxia) to the affected area.

Question 10

• Pathophysiology of acute renal failure, explaining signs and symptoms of the disease.

Answer 10

o Sudden decline in kidney function.

Split into - pre- impaired renal blood flow, intra- tubular necrosis, nephrotoxins, sepsis, post- urinary tract obstructions renal injury> decreased glomerular filtration rate (GFR).

 Reduced GFR> reduces the amount of filtrate being filtered therefore reducing urine output and increasing >BUN and Creatinine within the bloodstream >Oliguria, Increase in Blood urea nitrogen (BUN) & creatinine.

Question 11

Pathophysiology related to signs and symptoms of Glomerular Damage

Answer 11

Glomerular damage occurs, leading to impaired filtration of waste products and electrolytes.
Signs and symptoms: Proteinuria (protein in the urine), hematuria (blood in the urine), and decreased glomerular filtration rate (GFR), resulting in reduced urine output and fluid retention.

Question 12

Pathophysiology and related signs and symptoms of Tubulointerstitial Injury:

Answer 12

Damage to the tubules and interstitium of the kidneys can occur due to ischemia, inflammation, or nephrotoxic substances.
Signs and symptoms:
Impaired tubular reabsorption and secretion lead to electrolyte imbalances (e.g., hyperkalemia, hypocalcemia), metabolic acidosis, and disturbances in fluid balance.

Question 13

Pathophysiology and related signs and symptoms of o Renal Fibrosis

Answer 13

Progressive scarring and fibrosis of kidney tissue occur in response to ongoing injury and inflammation.
 Signs and symptoms: Gradual decline in kidney function, manifested by worsening azotemia.

Question 14

Pathophysiology and related signs and symptoms of Renal Hypoxia:

Answer 14

Reduced blood flow to the kidneys, often due to vascular abnormalities, exacerbates tissue hypoxia and contributes to further damage.

Signs and symptoms: Activation of the renin-angiotensin-aldosterone system (RAAS) leads to hypertension, exacerbating renal injury and contributing to cardiovascular complications.

Question 15

Pathophysiology and related signs and symptoms of o Fluid and Electrolyte Imbalance

Answer 15

Impaired kidney function >contributing to hypertension, edema, and electrolyte abnormalities.
 Signs and symptoms: Hypertension, edema, hyperkalemia (manifesting as muscle weakness, cardiac arrhythmias), and hyponatremia (manifesting as confusion, seizures)

Question 16

Explain the pathophysiology of acid base imbalance that can occur with kidney injury

Answer 16

GFR decreases> reduced hydrogen ion elimination and decreased bicarbonate reabsorption.
o Can regulate acid–base balance by secreting hydrogen into the urine and reabsorbing bicarbonate >↑ alkalinity of the plasma when the kidneys are damaged they are no longer able to do this causing a build up and causes an imbalance.

Question 17

Explain how hypernatremia can lead to neurological symptoms such as lethargy and irritability by relating it to cellular changes.

Answer 17

Sodium level content is too high in the extracellular fluid
Water will leave the intracellular space causing dehydration.
Causing shrinking in the brain tissue causing lethargy and irritability.

Question 18

Identify the type of intravenous fluid to manage hypernatraemia and explain why.

Answer 18

Give oral fluids or isotonic sodium-free fluid (5% dextrose in water) unit the sodium serum level is resorted bring it back to homeostasis.

Question 19

Identify two organs responsible for the short-term and long-term regulation of acid–base balance/

Answer 19

Kidney (Long term) and Lungs (Short term)

Question 20

Explain the underlying pathophysiology of acholic liver cirrhosis.

Answer 20

Alcohol is directly toxic to the liver> transported directly to the liver via hepatic portal vein > fatty liver steatosis> Alcoholic hepatitis >alcoholic cirrhosis. (irreversible changes)

Hepatomegaly, gastrointestinal hemorrhage, anemia, portal hypertension, hepatic encephalopathy, esophageal varices.

Question 21

• Explain the underlying complication of liver failure ascites

Answer 21

 cirrhosis,
 portal hypertension- Pressure exerted in vein pushes the fluid out and leads to accumulation of fluid in the peroneal space.
 Reduced albumin levels- Liver cannot produce enough albumin> water moves out of intravascular space into the interstitial space leading to acumination of fluid in the peritoneal cavity.

Question 22

explain hepatic encepalopothy

Answer 22

Liver dysfunction> blood shunted around liver to systemic circulation> toxins absorbed from GIT tract circulates to the brain (Ammonia)> affects neurotransmission, causing central nervouse system disturbances & alteratered consciousness.

Question 23

explain portal hypertension

Answer 23

Abnormally high blood pressure, Obstruction (cirrhosis) of blood flow through the portal venous system or vena cava (out of liver).> buildup of blood pressure before the liver.

Question 24

What are varacies

Answer 24

Distended veins> prolonged pressure in collateral veins> varices form (lower esophagus, stomach & rectum >rupture can be life threatening.

Question 26

explain liver cirrhosis

Answer 26

 portal hypertension- Pressure exerted in vein pushes the fluid out and leads to accumulation of fluid in the peroneal space.
 Reduced albumin levels- Liver cannot produce enough albumin> water moves out of intravascular space into the interstitial space leading to acumination of fluid in the peritoneal cavity.

Question 27

explain jaundice

Answer 27

Excess of bilirubin
 Prehepatic jaundice- excessive breakdown of red blood cells >Bilirubin is formed> exceeds the ability of the liver to metabolise bilirubin> blood levels rise > yellow pigmentation of skin and sclera.
 Intrahepatic jaunsince- disturbances in hepatocyte function and obstruction of bile canaliculi (diminished flow of metabolised bilirubin out of the liver into the common bile duct.)> metabolism of bilirubin is impaired> elevated in the blood and urine.

Question 28

• Explain the pathophysiology of hepatic encephalopathy. The most hazardous substance to the brain must be mentioned.

Answer 28

Liver dysfunction> blood shunted around liver to systemic circulation> toxins absorbed from GIT tract circulates to the brain (Ammonia)> affects neurotransmission, causing central nervous system disturbances & alterered consciousness.

Question 29

• Explain your nursing priorities when caring for a patient with symptomatic chronic liver cirrhosis.

Answer 29

• Management of NAFLD is primarily through lifestyle changes (may reserve the condition in early stage)
• Increasing physical activity, losing weight, a healthy diet
• Alcohol cessation (e.g. baclofen)
• Manage complications, such as:
• Ascites, Gastrointestinal bleeding, Encephalopathy- Lactulose (To manage Hepatic encephalopathy > it prevents ammonia absorption in the colon)
• With severe disease progression treated with: Corticosteroids, Antioxidants
• End-stage liver disease: Liver transplantation

Question 30

• Explain why conducting brain scans is essential before administering thrombolytic therapy for the treatment of an ischemic stroke.

Answer 30

o To determine the type of stroke and therefore the course of action that should be taken. If you give thrombolytics to a herhragic stroke you will increase the bleeding and put the patient at greater risk of death.

Question 31

Compare the pathophysiological difference between diffuse brain injury and focal brain injury.

Answer 31

focal brain in jury is typicaly in one area at the point of impact where diffused brain injury is widesoread damage with axonal injury.

Question 32

• Explain the pathophysiology of a coup contrecoup head injury.

Answer 32

Damage occurring at two opposite sides of the brain due to an initial impact (direct trauma), shearing force, trauma to base of brain. Followed by a rebound effect, impact within the skull hitting the opposite side of the skull, shearing force. Injury happens together in one continuous motion. Pathophysiology involves direct trauma to the brain tissue at the impact site (coup) and the opposite side due to rebound (contrecoup), leading to various neurological consequences and potential complications.

Question 33

• Describe the underlying pathophysiology of a cerebral vascular accident (CVA).

Answer 33

o Blood vessel supplying the brain with oxygen is altered> insufficient blood flow more than 5mins > death
o Hemorrhagic Stroke- bleeding from the cerebral vessels into brain tissue> haematoma is formed.
 Intracerebral haemorrhage- Other causes include bleeding into a tumour, haemorrhage associated with bleeding disorders, anticoagulation medications (substances that limit blood clotting), head trauma and illicit drug use.
 Subarachnoid haemorrhage- bleeding into the subarachnoid space that contains cerebrospinal fluid (CSF)> can cause a significant haematoma > increase in intracranial pressure.
o Ischemic stroke- blockage of cerebral vessels supplying brain tissue.3
 Thrombolytic stroke
* originates in the brain vessel
* Transient ischemic stroke- short term, partial or full obstruction of blood flow
 Embolic stroke- Clot originates from a vessel outside of the brain
* Thrombus forms and breaks away getting stuck in the brain causing a blockage.

Question 34

• Explain your nursing interventions including medications for a patient that has suffered a CVA.

Answer 34

o A – monitor airway patency, intubate patient unable to protect their airway from aspiration
o B- RR, Sp02 – 02 requirement
o C- pulse, BP
o D- GCS, pupil response, posturing – decorticate/decelerate
o BSL
o Pain score
o IV access, IVT
o Tests – CT scan, CXR, ECG
o Body positioning – side recovery position or high fowlers
o NBM – speech pathology RV to assess swallow
o Consideration of pathways for nutrition, may require enteral feeding via NGT.
* CT scan, blood test (serum levels for troponin I & INR) and a lumbar puncture (insertion of a needle into the subarachnoid space to sample the CSF). This CSF sample will identify if blood is present.
* Treatment is directed at controlling intracranial pressure, preventing ischemia and hypoxia of the neural tissues and preventing rebleeding.
* Medications include
o TPA- Thrombolytic agents to break up fibrin
o Anticoagulation therapy in ischemic stroke to prevent further strokes.

Question 35

• Explain the relationship between Herpes varicella and Herpes zoster.

Answer 35

o Herpes varicella and herpes zoster are both caused by the varicella-zoster virus, herpese varicella is the first instance of the virus and following the virus remains dormant in trigeminal and dorsal root ganglia> reactivation years later causes herpes zoster (Shingles).

Question 36

Explain the complications and nursing management of scabies.

Answer 36

o Scabies are highly contagious and is transmitted by skin-to-skin contact, contact with the likes of towels and bedclothes and can spread in close contact areas such as aged care facilities and wards. Contact precautions should be adhered to and PPE when nursing patient with scabies, as well as proper management of linen and personal hygiene items such as clothing and towels.

Question 37

• Explain the underlying pathophysiology of a burn injury.

Answer 37

Burns exceeding 20% of total body surface area leads to massive fluid shifts, oedema and release of inflammatory mediators.
o Inflammatory process > increased vascular permeability > plasma leaks out of the damaged capillaries into the surrounding tissues causing intravascular hypovolemia (low blood volume).
The loss of plasma proteins from the vascular space > hypoproteinaemia (low protein levels)> shift of electrolytes Hyponatraemia, hyperkalaemia/

Question 38

Metformin

Answer 38

Indications: T2DM

Mechanism: Closes ATP-sensitive Potassiom channels, preventing calcium entry and insulin secretion from pancreatic B cells. Increases number of insulin receptors, decrease insulin uptake by peripheral tissues and reduces hepatic gluconeogenesis

precautions: Stop 48 hours before and after radiologic studies and should be used cautiously in patients with impaired renal function.

ADVERSE EFFECTS: Diarrhea, nausea, vomiting, GI bloating.

INTERACTIONS: Cimetide, frusomide increase effects and alcohol intake increase lactic acidosis risk

Question 39

Actrapid
Lantus

Answer 39

CLASS: Antibiabetic agent/ Pancreatic hormone.
Indication: T1&2DM

Mechanism: facilitates removal of glucose from the blood into muscle and fat cells.

Precautions: Hyper or hypoglycaemia and other insulin products. Must be given on time in regiment.

Adverse reactions: Interacts with B-Blockers as they mask hypoglycaemia signs. Interacts with steroids, thyroid medications, rifampin, alcohol, NSAIDs and warfarin

Question 40

Glipizide

Answer 40

Class: Antibiabetic agent/ Pancreatic hormone.
Indications:T2DM
Mechanisms: Closes ATP-sensitive Potassiom channels, preventing K efflux and causing cell depolarisation, calcium entry and insulin secretion from pancreatic B cells. Increases number of insulin receptors, decrease insulin uptake by peripheral tissues and reduces hepatic gluconeogenesis.

Precautions: preganacy, G6PD deficiency, hypoglycaemia, hepatic or renal failure

ADVERSE EFFECTS: Hypoglycae,ia, weight gain, GIT and taste disturbance and rashes, Blood disorders and allergies.

INTERACTIONS: Other diabetic agents, CYP2C9 pathway drugs, alcohol, and drugs competing for protein binding sites(Thyroid, Diuretics, Steroids, phenytoin

Question 41

Loop diuretics

Answer 41

Class: Diuretic
Indications:LOOP: hypertension, hypercalcemia, heart failure, oedema. THIAZIDE: Hypertension, nephrogenic diabetes insipidus and nephrolithiasis POTASSIUM SPARRING: Hyperaldosteroneism, hypokalaemia. hypertension, severe heart failura
Mechanisms: OOP; Inhibits Na, K, 2Cl cotransporter into ascending limb of the loop of henle. Blocks Na and Cl reabsorption.
Precautions Hypokalaemia, hyperuricaemia, hypotension, metabolic acidosis, hypermagnesemia, stroke and coronary artery disease, cardiovascular complications
ADVERSE EFFECTS:
INTERACTIONS:

Question 41

Dapagliflozine

Answer 41

Class: Antidiabetic agent
Indications:T2DM

Mechanisms: inhibiting SGLT2 produces glycosuria (excess sugar in the urine) and osmotic diuresis, reduces hyperglycaemia and reduces weight and fluid load. Does not depend on insulin secreation or sensitivity.

Precautions: hepatics and renal impairment, ketoacidosis

ADVERSE EFFECTS: Urinary and genital tract infections, thirst, hypovolaemia, increased haematocrit and bone fractures risk
INTERACTIONS:

Question 42

Normal Saline
CSL
Gelofusin
albumin

Answer 42

Class: Fluids
Indications: Dehydration
Mechanisms: Fluids containing salts and minerals other than sodium in normal saline
Precautions:

ADVERSE EFFECTS:
INTERACTIONS:

Question 43

Loperamide

Answer 43

Class: Anti-diarrheal
Receptor: opioid receptor agonist.
Indications: diarrhea
Mechanisms: Binds to the opiod receptor wall in small intestine to slow motility and intestinal transit.
Precautions:

ADVERSE EFFECTS:
INTERACTIONS:

Question 44

Pantoprazole

Answer 44

Class:
Indications: Gastrointestinal lesions, Reflux, gastro-oesophageal.
Mechanisms: Selective proton pump inhibitor. Pantoprazole is converted to its active form and binds to the proton pump. This causes potent and long-lasting suppression of basal and stimulated gastric acid secretion irrespective of the stimulus.
Precautions:

ADVERSE EFFECTS: abdominal pain or tenderness; nausea; blood in stools; pale skin; tiredness or weakness [unusual])
INTERACTIONS:

Question 45

Mannitol

Answer 45

Class:
Indications: promotion of diuresis, in the prevention and/or treatment of the oliguric phase of acute renal failure, the reduction of elevated intraocular pressure and intracranial pressure and treatment of cerebral oedema as well as promoting the urinary excretion of toxic substances.
Mechanisms: Osmotic diuretic that causes diuresis by adding to the solutes already present in the tubular fluid. They reduce passive water reabsorption in the tubules and alters the electrochemical gradients less(less impact of electrolyte levels).

Precautions: DO NOT USE IF: severe heart failure or pulmonary congestion, severe dehydration, active intracranial bleeding, progressive renal or heart failure

Can cross the barrier and sit in the intisticial space and then the fluid can leak back into isticial space and increase plasma osmolarity and reverse osmosis.
INTERACTIONS:

ADVERSE EFFECTS:ADVERSE EFFECTS:cCNS toxicity, Nasuea vomiting, Local pain, hyper/hypotension, electrolyte shift and osmolarity imbalance, acidosis, oedema, incontinence, hyponatremia

Question 47

potasium sparing diuretics

Answer 47

Class: diuretics
Indication: Hyperaldosteroneism, hypokalaemia. hypertension, severe heart failura
Mechanism: Blocks aldosterone receptors, increases Na excretion and decrease K excretion.
Precautions Hypokalaemia, hyperuricaemia, hypotension, metabolic acidosis, hypermagnesemia, stroke and coronary artery disease, cardiovascular complications