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A Pathophysiology- BN607 > REVIEW LIST OF TEST 2- SPECIFIC! > Flashcards

REVIEW LIST OF TEST 2- SPECIFIC! Flashcards

1
Q

What is acute kidney injury (AKI)

A

Acute kidney injury (AKI) is a sudden decline in renal function resulting in a decreased ability to regulate fluid, electrolyte and acid-base balance.

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2
Q

How can kidney function be measured?

A

Kidney function can be measured by GFR, Urea, Creatine, and Oliguria (urinary output less than 400 ml per day)

Acute kidney injury is associated with a reduction of GFR by 25% or more, oliguria (in most cases) and retention of metabolic wastes, particularly azotemia. These changes typically occur within a few hours to days of the initial insult.

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3
Q

What can a acute kidney injury be categorised as

A

Acute kidney injury can be categorized based on
1) prerenal causes
2) intrarenal (intrinsic) causes
3) postrenal causes.

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4
Q

What is prerenal AKI? And what is it caused by?

A

Prerenal causes are the most common

Due to any cause of reduced blood flow to the kidney

Such as: hypovolemia (a state of low extracellular fluid volume, generally secondary to combined sodium and water loss), hemorrhage, hypotension, septic shock, etc.

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5
Q

What intrarenal (intrinsic) AKI?

A

Intrarenal (intrinsic) causes are due to abnormalities or complications within the kidney(s) itself. Intrinsic kidney damage

Such as: acute tubular necrosis; glomerulonephritis; polycystic kidney disease.

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6
Q

What is postrenal AKI?

A

Postrenal: Postrenal causes relate to complications within the renal tract that affect kidney function. Occurs after acute obstruction of the urinary flow, which increases intra-tubular pressure and thus decreases GFR

Such as: urinary tract obstructions; neurogenic bladder

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7
Q

What is symptoms of AKI?

A

1) Metabolic acidosis
2) Anuria (no urine, or without urine)
3) Fluid retention & oedema
4) Nausea/vomiting or anorexia
5) Various neurological manifestations such as irritability, drowsiness or confusion.

Eventually recovery begins to occur which sees a progressive return of normal function with a rise in GFR and urine output (diuresis) and falls in BUN and serum creatinine; though this may take a few to several months.

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8
Q

What are some management options for AKI

A
  • Maintenance of adequate fluid, electrolyte and acid-base balances
  • adequate nutrient intake
  • prevention/management of infection

Renal replacement therapy (dialysis) may be required if adequate fluid, electrolyte and acid-base balance is not maintained.

Consideration must also be given to any medications/drug therapy used by patients who develop AKI due to alterations in renal clearance occurring with the condition.

With timely and effective diagnosis, treatment of causes and adequate supportive management, recovery from AKI can occur, however, AKI also increases the risk for subsequent, or later, development of chronic kidney disease.

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9
Q

What is chronic kidney disease? CKD

A

Chronic kidney disease is a complex condition whereby there is progressive and irreversible destruction of nephrons.

There is a progressive reduction in GFR and subsequent reductions in nephron function and other kidney functions.

CKD progresses through stages, related to the progressive decline in GFR.

Because the kidneys have a great ability to adapt to nephron loss, symptomatic changes associated with chronic kidney disease occur gradually and may not become evident until much later in the disease.

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10
Q

What are the most common causes of CKD?

A

Diabetes mellitus
Hypertension
Glomerulonephritis
Polycystic kidney disease

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11
Q

What does the kidneys do to compensate for nephron loss?

A

The kidneys have a great ability to adapt to nephron loss. Symptomatic changes occur gradually and may not become evident until much later. The functioning nephrons adapt to extra ‘workload’ and continue to excrete relatively normal levels of water and solutes.

However, this extra workload results in the following changes to these adapting nephrons:
- Glomerular hypertension
- Glomerular hyperfiltration
- Glomerular hypertrophy
- Glomerulosclerosis (scarring)
- Tubulointerstitial inflammation & fibrosis

Thus, eventually these nephrons succumb to dysfunction and nephron loss continues to progress. End-stage kidney disease occurs when there is less than 10% of renal function remaining.

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12
Q

What are symptoms of CKD?

A

Due to the wide and varied effects of chronic kidney disease on body systems and body fluids, there are numerous signs & symptoms that eventually manifest with the disease.

Uremia (a buildup of waste products in your blood) is a syndrome of CKD characterized by azotemia and the accompanying systemic symptoms, including:
fatigue
anorexia
nausea/vomiting
weight loss
hypertension
pruritis
neurological, musculoskeletal & cardiovascular changes.

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13
Q

What is management for CKD?

A

Management of chronic kidney disease will depend on the stage of the disease. Generally in the early stages management is around trying to slow progression of the disease and may include

  • Dietary control with adequate calorie intake
  • Protein restriction
  • Vit D supplementation (When kidneys fail, their ability to activate vitamin D is lost)
  • Fluid evaluation
  • Sodium, potassium & phosphate restriction (Decrease bp and so levels arent to high)
  • Erythropoietin supplementation
  • ACE inhibitors or receptor blockers (Decrease bp)
  • Hyperglycemic control & insulin (for patients with diabetes)

When end-stage renal disease occurs, dialysis or renal transplant will be necessary for survival.

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14
Q

What is a urinary tract obstruction?

A

Obstruction of urinary flow occurring anywhere from the renal calyces to the urethra. The obstruction may be anatomical or functional

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15
Q

What could a urinary tract obstruction be caused by?

A
  • Kidney/renal stones (calculi) (Most common)
  • Compression from other structures (Tumour, nearby inflammation)
  • Stricture or stenosis (narrowing) of tract
  • Vesicoureteral reflux (urine flows from bladder back into ureters)
  • Prostatic hypertrophy (compresses the urethra)
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16
Q

What does a urinary tract obstruction cause?

A

Obstruction results in dilation of the tract proximal to the obstruction and the accumulation/ backflow of urine-
hydroureter and/or hydronephrosis.

Backup first affects the distal nephron, then proximal nephron and eventually the glomeruli, causing damage and reduction in kidney tissue.

The damange can subsequntly lead to:
- Decreased GFR
- Decreased reabsorption & urine concentration (so initially increased urine production)
- Decreased secretion (can lead to metabolic acidosis)

Can ultimately lead to acute kidney injury (and subsequently chronic kidney disease).

Obstruction and the accumulation of urine increases the risk of infection.

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17
Q

What is hypernatremia? and what is it caused by?

A

Increased sodium levels in the blood.

Most commonly caused by water loss, but can also be caused by excessive sodium gain in the ECF. This leads to an increase in plasma osmolarity, which, if not corrected, will result in a fluid shift of water from the ICF to the ECF, leading to cellular dysfunction.

Causes hypertonic cells.

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18
Q

What are the main symptoms of hypernatremia?

A
  • Increased thirst (polydipsia)
  • Dry mucous membranes
  • CNS symptoms of cellular dysfunction, including: lethargy, irritability, muscle twitching/convulsions, seizures and possibly coma
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19
Q

What is respiratory acidosis

A

If the pH is below 7.35 and the problem is caused by our breathing.

PH levels below 6.8 are fatal

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20
Q

What causes respiratory acidosis

A

Too much CO2 in blood= acidotic

Trigger not sensed:
1) Depression of brainstem respiratory centre from brain trauma, damage, tumor, or ischemia (decrease RR)
2) Sedative drugs- opioids & benzodiazepine

Response inadequate:
1) Decreases neuromuscular control of ventilation. Can be from guillain- barre, exhaustion, rib fractures that stop deep breathing

Airway obstruction:
COPD, pneumonia, asthma, bronchitis, increased airway resistance, HF, blockage with tongue. CO2 trapping.

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21
Q

What are symptoms of respiratory acidosis? (8)

A

Symptoms
- Blurred vision ★
- Breathlessness ★
- Convulsions
- Disorientation ★
- Headache
- Lethargy
- Muscle twitching ★
- Tremors ★

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22
Q

What is Respiratory Alkalosis

A

If the pH is above 7.45 and the problem is caused by our breathing

PH levels higher than 7.8 are fatal

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23
Q

What causes Respiratory Alkalosis

A

Hyperventilation. Blowing out your acids. To much CO2 expelled, not enough H+, increase blood PH

Tachypnea is increase of RR. Hyperventilation is not enough CO2.

Hypoxic drive
(Body trying to get more O2). Can be from pneumonia, pulmonary embolism, congestive HF

Non Hypoxic drive
Pain, agitation, fear, fever, spesis

Some head injuries. Alkalosis lowers the pressure in the head, so the body may make itself alkalotic if pressure is building in the head.

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24
Q

What are symptoms of respiratory alkalosis? (5)

A

Symptoms
- Confusion
- Convulsions
- Dizziness ★
- Muscle spasms ★
- Paraesthesia (tingling sensation) ★

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25
Q

What is Metabolic alkalosis?

A

If the pH is above 7.45 and the problem is caused by our kidney or our body

PH above 7.8 are fatal.

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26
Q

What causes Metabolic alkalosis?

A

Increased loss of H+

Renal loss of H+
From diuretics (make the kidneys get rid of acid), increased liquorice ingestion, cushing syndrome. Hyperaldosteronism (causes kidneys to reabsorb Na+ but lose both H+ and K+)

Intrarenal loss= vomiting

Increased bicarb retention (Not common). Caused by overtreatment of IV bicarb solution to correct acidosis.

Dehydration causes both acid loss and bicarb retention.

Post hypercapnic bicarb retention.

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27
Q

What are the symptoms of metabolic alkalosis? (7)

A

Symptoms:
- Atrial tachycardia ★
- Confusion
- Convulsions
- Hyper-reflexia ★
- Hypoventillation ★
- Muscle cramps ★
- Tetany ★
- Weakness ★

Metabolic alkalosis causes calcium to bind to proteins, so there is less calcium in the blood.

The symptoms of metabolic alkalosis will be the same as hypocalcaemia

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28
Q

What is Metabolic acidosis

A

If the pH is below 7.35 and the problem is caused by our kidney or our body, we call it

PH below 6.8 are fatal

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29
Q

What causes metabolic acidosis?

A

Increased bicarb loss (normal anion gap metabolic acidosis)
- Can be caused from renal loss (Renal failure). Kidneys make bicarb from ammonia metabolism. Renal failure ↓ metabolism ↓ bicarb production. Also not as good at filtering acid.
- GI loss. Can be from diarrhea & pancreatitis

Increased acid production (Increased anion gap metabolic acidosis)
- Can be from ↑ lactic acid production (↑ anaerobic respiration due to ischemia or Hypoxemia)
- Ketoacidosis. Body metabolised fat for energy, which releases ketones (acid). Caused by alcohol, diabetes, starvation.
- Increased exposure to toxic substances.
- Certain medications (Paracetamol and aspirin)
- Extreme exercise

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30
Q

What are symptoms of metabolic acidosis? (10)

A

Symptoms:
- Arrhythmias
- Confusion
- Coma
- Diarrhea
- Fast, deep breathing to try to blow out the acid
- Headache
- Hypotension
- Kussmaul respirations (deep and labored breathing)
- Lethargy
- Nausea/ vomiting

The symptoms of metabolic acidosis often occur with hypokalaemia. Metabolic acidosis also makes hypokalaemia more dangerous.

31
Q

What is cushing syndrome?

A

Cushing’s syndrome refers to the signs and symptoms of chronic excessive cortisol levels (hypercortisolism).

32
Q

What is the negative feedback that maintains normal cortisol levels?

A

Excess free cortisol is filtered by the kidneys and excreted in the urine.

High cortisol tells the hypothalamus & the pituitary gland to decrease their secretion of CRH & ACTH. Less CRH reduces the amount of ACTH produced by the pituitary gland. Less ACTH means the zone of fasciculata (adrenal gland) gets less stimulation to make cortisol.

33
Q

What causes cushing syndrome?

A

Exogenous (outside)
Medications- Steroids act similar to cortisol in the respect that they mimic action on tissue.
→ To much medication/ cortisol causes negative feedback on the hypothalamus
→ which shuts down cortisol production in the zone of fasciculata
→ lack of stimulation over time can cause the zone to shrink
→ Although it causes less endogenous production still does not compensate for the huge levels of exogenous cortisol, which causes cushing syndrome to develop.

Endogenous (inside- made by the body)
→ Excess ACTH most commonly from a pituitary adenoma (benign tumour) this is specifically called CUSHING DISEASE.
→ Small lung cancer → Excess ACTH
→ Tumours of the adrenal gland. Adrenal adenoma (benign) and adrenal carcinoma (malignant). Cells in the zone of fasciculata divide abnormally and secrete excess cortisol. As a result their is a decrease in CRH and ACTH production which shrinks the adrenal gland and makes less cortisol. Net result: cushing syndrome.

34
Q

What are symptoms of cushing disease?

A

Symptoms-
- Muscle wasting and thin extremities
- Easy bruising
- Abdominal striae (Kind of like stretch marks)
- Fractures (bone deterioration)
- Full mood shaped face
- Dampened inflammatory and immune response
- Buffalo hump
- Impaired normal brain function
- Truncal obesity
- Messes up normal ovarian and testicular function
- Hyperglycemia - can lead to diabetes, hypertension, increased risk for cardiovascular disease, increase risk of infections, poor wound healing, amenorea, psychiatric or mental disturbances.

35
Q

How can you diagnose cushing disease?

A

Diagnosis- measuring free cortisol (24 hour urine sample). Blood and salvia tests late at night

36
Q

What is hyperthyroidism? And what does it cause?

A

Hyperthyroidism is the production of too much thyroxine hormone (T4).

High circulating levels of TH causes thyrotoxicosis: A hypermetabolic state directly related to an increased BMR and associated increased sympathetic nervous system activity

Causes an increased growth of the thyroid gland (goiter) with an increased blood supply and increased iodine uptake to sustain the increased TH production & storage. A rare, but life-threatening , complication of hyperthyroidism is athyroid storm.

37
Q

What are causes of hyperthyroidism?

A
  • Grave’s disease causes hyperthyroidism in over 95% of cases

Other rarer causes include
- Toxic adenoma
- Toxic multinodulargoiter (Enlargement of thyroid gland)
- Thyroiditis (Inflammation).

Grave’s disease is an autoimmune condition where B-lymphocytes produce IgG antibodies which mimic TSH.These auto-antibodies bind to TSH receptors and induce increased production and secretion of TH.

38
Q

What are symptoms of hyperthyroidism?

A
  • Weight loss
  • Increased growth of the thyroid gland (goiter)
  • Increased appetite
  • Nervous, irritable and anxious
  • Palpitations and tachycardia
  • Heat intolerance
  • Restlessness or insomnia
  • Warm, moist skin
  • Tremor & muscle weakness
39
Q

How can obesity lead to respiratory complications?

A

Increases in fat around the chest & abdomen decrease expansion of the thorax leading to obstructive sleep apnoea

Asthma has been associated with obesity, though the mechanism is unknown (possibly linked to alterations in immunity associated with adipocytokine dysregulation)

40
Q

How do you measure obesity?

A

Obesity is classified using the body mass index (BMI) calculation which measures weight/height2 (kg/m2).

Underweight- < 18.5
Healthy weight- 18.5 - 24.9
Overweight- 25.0 - 29.9
Obese (Class I)- 30.0 - 34.9
Obese (Class II)- 35.0 - 39.9
Obese (Class III) > 40.0

Class II obesity is sometimes referred to as extremely obese, while class III obesity is sometimes referred to as severely or morbidly obese.

BMI calculations do NOT take into account body composition (e.g. fat mass vs. muscle mass)

41
Q

What are additional measures used to determine/diagnose obesity?

A

anthropomorphic measures such as:
- waist circumference
- skin fold thickness
- waist to hip ratio

body scans such as CT, MRI or DEXA (Fat mass index measured via DEXA scan)

hydrostatic weighing (Underwater weighing)

42
Q

What is the goal of fluid resuscitation in burn injuries?

A

The primary role of fluid resuscitation is to maintain organ perfusion (hemodynamics) and substrate (oxygen, electrolytes, among others)

Perfusing kidneys goal of IV therapy (mL/min/g).

If kidneys perfused, the patient will make enough urine.

43
Q

What are special considerations for fluid resuscitation for burn victims?

A

If kidneys perfused, the patient will make enough urine. If patient doesn’t make enough urine they’re not getting enough fluid. Even if resuscitation guidelines are followed, some people require more fluid. Check! May need to turn rate of IV fluid up, DON’T GIVE DIURETICS!

Patients with electrical injuries or very deep tissue damage may have myoglobin in urine, will require double the urine output to flush kidneys of large myoglobin cells. If urine very dark, increase rate of IV fluids to maintain urine output of 100 ml/hr.

44
Q

What is the most commonly used liquid for fluid resuscitation? And what is in it?

A

Lactated Ringer’s is most like normal extracellular fluid and is fluid of choice (sodium chloride, sodium lactate, potassium chloride, and calcium chloride in water.)

45
Q

What is the parkland formula (most common) used for and what is the formula for adults

A

Currently, the Parkland formula is the most frequently used burn resuscitation formula.

Adults-
TBSA: Total body surface area
4ml x TBSA (%) x body weight (kg)
50% given in first 8 hours
50% given in next 16 hours

46
Q

What is the parkland formula for children?

A

Children receive maintenance fluid in addition, at an hourly rate of:
4ml/kg for the first 10kg of body weight plus
2ml/kg for the second 10kg of body weight plus
1ml/kg for >20kg of body weight

47
Q

What is the end point of fluid resuscitation?

A

When a person is producing enough urine output

Urine – adults: 0.5–1.0 ml/kg/hour

Urine – children: 1.0–1.5ml/kg/hour

48
Q

How do you assess burn area?

A

Initial assessment- wallace rule of nines
Adult: Head 9%, arms 9%, front chest/ trunk 18%, back chest/ trunk 18%, legs 18%, groin 1%

Children: 18% head, arms 9%, front chest/ trunk 18%, back chest/ trunk 18%, legs 14%, groin 1%

Secondary assessment- Lund and browder chart

49
Q

What are local affects for burns? (6)

A
  • Pain
  • Vasodilatation
  • Increased capillary permeability with loss of albumin into interstitial spaces (ISS)
  • Loss of fluid and electrolytes into ISS and environment
  • Loss of heat due to conduction and evaporation
  • Loss of protective skin barrier
50
Q

What are systematic affects for burns? (15)

A
  • Hypovolaemia (A condition in which the liquid portion of the blood (plasma) is too low)
  • Hypermeability of capillaries
  • Vasodilatation, release of inflammatory mediators
  • Immune response to burn
  • Infiltration of tissue with WBC
  • Stress ulceration
  • Bone marrow suppression
  • Loss of GIT barrier function
  • Deficiency of neutrophils may cause fatal infections
  • Heat induced (60 °C) denaturing of collagen fibers
  • In interstitium, causes extravasation of fluid
  • Hypermetabolic state (release of stress hormones)
  • glucagon, cortisol, catecholamines
  • Suppression of insulin, growth hormone & anabolic steroids
  • Widespread whole body changes
51
Q

What is Hypervolaemia?

A

A condition in which the liquid portion of the blood (plasma) is too high. Also known as fluid overload

52
Q

What are symptoms to hypervolaemia?

A

Hypertension
Tachycardia
Raised JVP - gallop rhythm
Oedema
Pleural effusions
Pulmonary oedema
Ascites
Organ failure

53
Q

What is Hypovolaemia

A

A condition in which the liquid portion of the blood (plasma) is too low. A state of abnormally low extracellular fluid in the body

54
Q

What are symptoms of hypovolaemia

A

Postural hypotension
Tachycardia
Absence of JVP@45 degrees
Decreased skin turgor
Dry mucosae
Supine hypotension
Oliguria (reduced urinary output)
Organ failure

55
Q

Whats Isotonic is terms of osmosis?

A

An isotonic solution is one that has the same concentration of solutes both inside and outside the cell

56
Q

Whats Hypotonic is terms of osmosis?

A

A hypotonic solution has a lower solute concentration compared to the intracellular solute concentration

Hypotonic(less concentrated comparative to plasma)

Hypo= hipo= fat

57
Q

What solutions are Isotonic?

A
  • 0.9% NaCl
  • Lactated Ringer’s
  • 5% dextrose and water (D5W)
  • 5% dextrose and 0.9% saline (various formulations)
58
Q

Whats Hypertonic is terms of osmosis?

A

A hypertonic solution has a higher solute concentration compared to the intracellular solute concentration.

Hypertonic(more concentrated comparative to plasma)

Hyper=active=skinny

59
Q

What solutions are Hypotonic?

A
  • 0.45% sodium chloride
  • 0.33% sodium chloride
60
Q

What solutions are Hypertonic?

A
  • 3% NaCl
  • Protein solutions
61
Q

Where does alcohol get metabolized?

A

Most of the alcohol in the bloodstream (>90%) will be metabolised by body structures- mostly by the liver, but also the pancreas, stomach & brain. The remaining alcohol is excreted in sweat, urine and via ventilation.

62
Q

What is the process of alcohol metabolism?

A

1) Ethanol is broken down into acetaldehyde by the enzyme alcohol dehydrogenase.

2) Acetaldehyde is a toxic substance that is a known carcinogen, but is relatively short-lived. Acetaldehyde is further broken down by the enzyme aldehyde dehydrogenase into the non-toxic acetate.

3) Acetate can then be broken down into carbon dioxide and water which can be eliminated from the body.

Ethanol may also be broken down by the cytochrome P450 2E1 (CYP2E1) enzyme. The metabolism of alcohol via this pathway can produce reactive oxygen species (ROS) which can lead to oxidative stress and subsequent tissue damage.
Only so much ethanol can be metabolized at a time- about one standard drink per hour. When plasma levels of ethanol exceed the metabolic capacity, then all of the ethanol cannot be metabolized and eliminated properly.

63
Q

If ethanol isn’t metabolised efficiently what can it lead to?

A

When it cannot be metabolized and eliminated effectively, it can lead to cell/tissue/organ injury via:

  • Inflammation
  • Oxidative stress
  • Protein modifications
  • Metabolic disruptions (i.e. impaired anabolic signaling, enhanced catabolic processes, dysregulation of lipid metabolism and signaling)
  • Imbalanced neurotransmission and neuroadaptive changes
64
Q

What is mild alcohol withdrawal?

A

Withdrawal symptoms are typically the opposite of the symptoms of intoxication. Involves the limbic system.

Hangover is a mild form of withdrawal after an acute intoxication
- Craving
- Headache
- Photosensitivity
- Vertigo
- Nystagmus
- Myalgia
- Nausea and vomiting
- Tachycardia
- Hypertension
- Diaphoresis
- Tremor
- Insomnia
- Anxiety
- Pallor
- Polydipsia

65
Q

What is SEVERE alcohol withdrawal?

A
  • Delirium tremens – most severe form of alcohol withdrawal
  • Complete confusion
  • Physical agitation
  • Visual and/or auditory and/or tactile hallucinations
  • Diaphoresis
  • Fever
  • Tachycardi
  • Hypertension

This can lead to circulatory collapse and death. In addition to the symptoms caused by the autonomic nervous system, many of the symptoms of alcohol withdrawal also come from dehydration, hypoglycaemia, and electrolyte imbalances, and acetaldehyde (Bryant, 2019) * CIWA Scale (Clinical Institute Withdrawal Assessment for Alcohol) is used in hospitals to assess severity of withdrawal

66
Q

Whats the CIWA SCALE?

A

Looks at the evidence that a client in detox from alcohol is starting to have a sympathetic nervous system reaction and is going into delirium tremens.
First assess pulse and blood pressure. What would you expect if the sympathetic nervous system is involved?

Then it gives a scale to assess: Nausea and vomiting; Tactile hallucinations; Tremor; Auditory hallucinations; Sweating and diaphoresis; Visual hallucinations; Anxiety; Headache; Agitation; Change in orientation.

67
Q

What are the different kinds of shock?

A

Distributiveshock; that is, they result from a problem with the distribution of blood throughout the circulatory network.
1. Neurogenic shock
2. Septic shock
3. Anaphylactic shock

Other
4. Cardiogenic shock
5. Hypovolemic shock
6. Obstructive shock

68
Q

What is shock?

A

Shock occurs when the cardiovascular system fails to maintain adequate tissue perfusion, resulting in widespread impairment of cellular metabolism and function.

Decreased cellular oxygen leads to anaerobic respiration
Decreased cellular glucose leads to alterations in glucose metabolism
Ultimately cellular dysfunction & damage leads to the following and the cycle of cell damage and dysfunction continues

69
Q

What is Cardiogenic shock?

A

Cardiogenic shock occurs when there is a decreased cardiac output, even in the presence of adequate blood volume, which results in tissue hypoxia.

  • myocardial infarction (MI)- most common
  • myocarditis
  • cardiomyopathy, etc
70
Q

What is Obstructive shock

A

Obstructive shock occurs when there is a decreased cardiac output related to obstruction or restriction of blood flow through the great vessels of the heart.

  • significant pulmonary embolism
  • pulmonary hypertension
71
Q

What is Hypovolemic shock

A

Hypovolemic shock occurs when there is a significant decrease(about 15% or more)in circulating blood volume due to fluid loss.

  • hemorrhage
  • plasma loss, as occurs with burns
  • dehydration
  • severediaphoresis, vomiting or diarrhoea
72
Q

What is Neurogenic shock

A

Neurogenic shock, also called vasogenic shock, occurs when there is widespread vasodilation associated with increases in parasympathetic stimulation and inhibition of sympathetic stimulation.

  • medulla (brainstem)or spinal cord injury
  • decreased oxygen or glucose supply to medulla
73
Q

What is Anaphylactic shock

A

Anaphylactic shock occurs when there is a hypersensitive reaction (anaphylaxis)to an allergen.

  • peanuts
  • shellfish
  • Insect venom
  • Latex
  • Penicillin
74
Q

What is Septic shock

A

Septic shock is part of the continuum of sepsis (infectiousmicroorganismsin the blood) in which circulatory and cellular metabolic abnormalities significantly increase morbidity.

A Pathophysiology- BN607 (28 decks)

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