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Extra GU Flashcards

1
Q

BPE

A

Benign prostatic enlargement-

This is a physical examination that is a CLINICAL DIAGNOSIS

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2
Q

BPH

A

Benign prostatic hyperplasia-

The no of cells increases and it is a HISTOLOGICAL DIAGNOSIS

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3
Q

BOO

A

Bladder outflow obstruction-

This is a urodynamic diagnosis

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4
Q

Hydronephrosis

A

Dilation of the renal pelvis of the kidney- leading to damage

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5
Q

Obstructive uropathy

A

Functional or anatomical obstruction of urinary flow at any level of the urinary tract.

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6
Q

Supravesical obstruction

A

ABOVE the level of the bladder

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7
Q

Infravesical obstruction

A

BELOW the level of the bladder

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8
Q

LUTS: give the 4 storage symptoms

A

1) Urgency
2) Nocturia (>30% voided volume at night)
3) Frequency
4) Overflow incontinence

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9
Q

LUTS: give the 7 voiding symptoms

A

1) Poor intermittent stream
2) Hesitancy (difficulty initiating urine)
3) Incomplete emptying
4) Post micturition dribbling
5) Straining
6) Haematuria
7) Dysuria

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10
Q

What is dysuria?

A

Painful urination

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11
Q

What are the red flags in LUTS?

A

Infection, stones or cancer

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12
Q

Serum prostate-specific antigen (PSA)

A
  • PSA is a glycoprotein that is expressed by normal and neoplastic prostate tissue.
  • Produced by the prostate in semen
  • Small amounts in the bloodstream normally
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13
Q

When can the PSA be raised?

A
  • BPH
  • Prostate cancer
  • Perianal trauma (post endoscopy/surgery)
  • BMI<25
  • Taller men
  • Recent ejaculation
  • Prostatitis
  • UTI
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14
Q

What value of PSA confers an increased risk of LUTS progression?

A

> 1.4ng/ml

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15
Q

What is a Max flow rate <10ml per second suggestive of?

A

Suggestive of bladder outflow obstruction due to BPH

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16
Q

What is the frequency volume chart?

A

Measure volumes voided and time over a minimum of 3 days. Determines whether polyuric or nocturic.

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17
Q

Bladder drill

A

Training the bladder to become less overactive

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18
Q

Indications for surgery for LUTS

RUSHES

A 
Retention
UTI's
Stones
Haematuria
Elevated creatinine due to bladder outflow obstruction
Symptoms deterioration
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19
Q

What is castration? Why is it protective against BPH?

A

Castration is the removal of testicles. Androgens e.g. testosterone do not cause BPH but are a requirement for BPH. BPH is not seen in those with castration prior to puberty or genetic disease that inhabit androgen action or production.

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20
Q

Describe the pathophysiology of BPH?

A
  • You will get a benign nodular or diffuse proliferation of musculofibrous and glandular layers of the prostate.
  • Inner (transitional) zone enlarges in contrast to peripheral layer expansion seen in prostate carcinoma
  • As the prostate enlarges, it may squeeze or partly block the urethra
  • This often causes problems with urinating.
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21
Q

What is the frequency volume chart?

A

Measures volumes voided and time over a minimum of 3 days. It calculates whether nocturic (>30% voided volume at night).

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22
Q

What are some side effects of tamsulosin?

A
  • drowsiness
  • dizziness
  • depression
  • ejaculatory failure
  • extra-pyramidal signs
  • weight increase
  • nasal congestion
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23
Q

When is Tamsulosin contraindicated?

A

In postural hypertension

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24
Q

What are the indications for surgery in BPH?

A
  • Large prostate
  • Failure to respond to an adequate trial of medical therapy
  • Acute urinary retention
  • Failed voiding trials
  • Recurrent gross haematuria
  • Renal insufficiency signs
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25
Q

Side effects of 5-alpha-reductase inhibitor

A
  • Impotence

- Decreased libido

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26
Q

Name some late and immediate risks of Transurethral resection of prostate.

A

Immediate:

1) bleeding
2) sepsis
3) retention
4) post TURP syndrome

Late:

1) retrograde ejaculation
2) incontinence
3) erectile dysfunction

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27
Q

What is the other surgical option for BPH?

A

Transurethral incision of the prostate

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28
Q

What is obstructive uropathy?

A

Obstructive uropathy is blockage of urinary flow, which can affect one or both kidneys depending on the level of obstruction. If only one kidney is affected, urinary output may be unchanged and serum creatinine can be normal. When kidney function is affected, this is termed obstructive nephropathy.

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29
Q

Name the different types of obstructive uropathies

A
  • Partial, complete, unilateral or bilateral
  • Luminal
  • Mural
  • Extramural
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30
Q

Name the causes of Luminal urinary obstruction

A
  • Stones
  • Blood Clot
  • Sloughed papilla
  • Tumour
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31
Q

Name the causes of mural urinary obstruction

A
  • Congenital or acquired stricture
  • Neuromuscular dysfunction
  • Schistomiasis
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32
Q

Name the causes of extramural urinary obstruction

A
  • Abdominal or pelvic mass/tumour
  • Retroperitoneal fibrosis
  • BPH
  • Prostate cancer
  • Pregnancy
  • Inflammation e.g. peritonitis or diverticulitis
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33
Q

What is classed as upper urinary tract?

A

Kidneys and ureter

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34
Q

What is classed as lower urinary tract?

A

Bladder to urethra

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35
Q

Name 2 advantages of a suprapubic catheter

A
  • Less risk of urethral damage and thus UTI

- Less likely to be colonised by bacteria than a long term urethral catheter

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36
Q

Name 2 disadvantages of a suprapubic catheter

A
  • Requires general anaesthetic for insertion

- Small risk of bowel injury during insertion

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37
Q

Name a disadvantage for a urethral catheter

A

Long term urethral catheter can lead to urethral erosion and damage to the urethral sphincter

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38
Q

How can urine obstruction relief lead to large diuresis?

A

After obstruction relief, it can result in temporary salt-losing nephropathy resulting in weight loss therefore you have to monitor weight and maintain fluid balance

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39
Q

What is the pathophysiology of Renal Cell Carcinomas?

A

-The mutation of the same tumour supressor gene is thought to be effected in RCC as in Von Hippel Lindau disease.

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40
Q

Name 4 places that renal cell carcinoma might metastasise to.

A

1) Lymph
2) Bone
3) Liver
4) Lungs

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41
Q

What percentage of people have metastases at the presentation?

A

25%

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42
Q

5 cancers that can metastasise to the bone?

5 B’s

A

1) Breast
2) Bronchus
3) Byroid (thyroid)
4) Brostate (Prostate)
5) Bidney (Kidney)

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43
Q

Why might renal cell carcinoma cause left-sided varicocele?

A

Rarely, invasion of the LEFT RENAL VEIN results in large compression of the LEFT GONADAL VEIN as the tumour will block where the gonadal vein drains into the renal vein.

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44
Q

What is the radiological lookalike of a renal cell carcinoma?

A

Xanthogranulomatous pyelonephritis

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45
Q

Wilm’s Tumour (NEPHROBLASTOMA)

  • What is it?
  • Presentation
  • Diagnosis
  • Treatment
A
  • Most common renal cancer in children
  • Abdominal mass and less commonly haematuria
  • CT, Ultrasound and MRI
  • Combination of nephrectomy, radiotherapy and chemotherapy.
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46
Q

Why is CT abdomen and chest with contrast the gold standard for renal cell carcinoma?

A
  • More sensitive than ultrasound in detecting mass
  • Shows involvement of renal vein via IVC to show any pulmonary mets
  • Contrast demonstrates kidney function as in a normal kidney you should see it being taken up and excreted well.
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47
Q

Negative of Ablative techniques like radiotherapy?

A

Can harm kidney function

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48
Q

BLADDER CANCER

A

///

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49
Q

Describe the pathophysiology of the spread of bladder cancer

A

Local: to pelvic structures
Lymphatic: to iliac and para-aortic nodes
Haematogenous: to liver and lungs

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50
Q

What is M-VAC chemotherapy?

A

Combination chemotherapy using methotrexate, vinblastine, adriamycin and cisplatin

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51
Q

What is CMV chemotherapy?

A

Cisplatin, methotrexate and Vinblastine

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52
Q

Name 3 nephrological causes of non-visible haematuria

A

1) IgA nephropathy
2) Thin basement membrane disease
3) Vasculitis

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53
Q

Name 3 common urological causes of non-visible haematuria

A

1) BPH
2) Cancer
3) Stone disease

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54
Q

Name 3 less common urological causes of non-visible haematuria

A

1) Radiation cystitis
2) urethral stricture
3) TB

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55
Q

Name 3 rare urological causes of non-visible haematuria

A

1) Renal artery thrombosis
2) Polycystic kidney disease
3) Renal papillary necrosis

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56
Q

What is a hydrocele?

A

A hydrocele is a type of swelling in the scrotum that occurs when fluid collects in the thin sheath surrounding a testicle.

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57
Q

AKI

A

/////

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58
Q

What is AKI?

A

An abrupt decrease in kidney function and GFR measured by serum creatinine increase and/or urine outflow reduction, occurring over days-hours.
It causes retention of ammonia and uric acid and dysregulation of extracellular volume and electrolytes.

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59
Q

What is the KDIGO classification for AKI?

A

Increase in serum creatinine >0.3mg/dL within 48 hrs
OR
Increase in serum creatinine 1.5x basal serum creatinine (best figure within 7 days)
OR
Urine volume of >0.5mL/kg/h for more than 6 consecutive hours

60
Q

CKD

61
Q

How does diabetes cause CKD?

A
  • Increase in blood glucose causes non-enzymatic glycosylation of efferent arterioles.
  • Causes efferent arterioles to get more stiff and more narrow, this creates an obstruction for blood to leave the glomerulus and increases pressure here by hyperfiltration.
  • The mesangial cells, in response to this, secrete more and more structural matrix
  • Over many years this process of glomerulosclerosis, diminishes the nephron’s ability to filter the expanding size of the glomerulus and leads to CKD
62
Q

How does hypertension cause CKD?

A
  • The walls of the arteries supplying the kidney begin to thicken in order to withstand the pressure» narrow lumen»»less blood and oxygen&raquo_space;>ischaemia in nephrons
  • Immune cells like macrophages and fat-laden macrophages called foam cells slip into the damged glomerulus and start secreting growth factors like TGF-BETA1
  • This causes mesangial cells to regress to immature mesangioblasts and secrete extracellular structural matrix»>GLOMERULOSCLEROSIS, SCARRING, HARDENING&raquo_space;>decreased ability to filter»>CKD
63
Q

Why is it a vicious cycle in CKD with hypertension?

A

The kidney senses lowering of GFR so respond by setting off the renin-angiotensin system. Angiotensin II has effect on podocytes and mesangial cells by increasing pore size so impairs size-selective function of the basement membrane for protein» protein urea. In CKD the falling GFR leads to more and more renin secretion»>hypertension»more damage

64
Q

What some indications for dialysis?

A

1) Symptomatic uraemia including pericarditis or tamponade
2) Hyperkalaemia not controlled
3) Pulmonary oedema/ hypervolemia that is not treated with diuretics
4) Arrhythmias on ECG
5) Metabolic acidosis

65
Q

RENAL VASCULAR DISEASE

66
Q

What is renal venous thrombosis?

A

Occlusion of one or both renal veins by a thrombus

67
Q

Name 5 causes of renal venous thrombosis?

A
  1. Nephrotic syndrome
  2. Renal cancer
  3. Renal transplant
  4. Dehydration
  5. Trauma
68
Q

What are the symptoms of RVT?

A

Symptoms may be difficult to differentiate from those of the underlying condition.

69
Q

What is the treatment and management for RVT?

A

Anticoagulation with WARFARIN

STREPTOKINASE can be used to lyse acute thrombosis

70
Q

Complications of RVT?

A
  1. AKI

2. Recurrent thromboembolism

71
Q

What is glomerulonephritis?

A

Is an umbrella term that refers to a group of parenchymal kidney disease that results in the inflammation of the glomeruli and nephrons.

72
Q

Nephrotic syndromes

A

LOTS OF PROTEIN
NO BLOOD
LOTS OF OEDEMA

73
Q

Nephritic syndromes

A

Some protein

LOTS OF BLOOD

74
Q

Why do you get severe oedema in nephrOtic syndromes?

A

The proteins lost in the urine are mainly albumins which result in hypoalbuminaemia; this causes oedema as there is a lower osmotic pressure within the vessels causing fluid to accumulate in the interstitial tissue fluid.

75
Q

Describe the pathophysiology behind nephrotic syndromes

A
  1. Injury to podocyte appears to be the main cause of proteinuria.
  2. Podocytes wrap around the glomerular capillaries and maintain the filtration barrier-preventing large molecular weight proteins from entering the urine
  3. Damage to podocyte foot processes or loss of podocytes can cause heavy proteinuria
76
Q

How would you differentiate between Congestive heart failure and Nephrotic syndromes?

A

CHF: oedema and RAISED JVP

Nephrotic syndromes: oedema and NORMAL/LOW JVP

77
Q

How would you differentiate between cirrhosis and Nephrotic syndromes?

A

In cirrhosis there is hypoalbuminaemia and oedema but there will also be signs of chronic liver failure e.g. jaundice, fever and loss of body hair.

78
Q

Why is there susceptibility to infection with nephrotic syndromes? e.g. cellulitis, streptococcus infections and spontaneous bacterial peritonitis

A
  • Low serum IgG, decreased complement activity and reduced T cell function due to loss of immunoglobulins in urine and also immunosuppressive treatment.
79
Q

Why is there susceptibility for thromboembolism with nephrotic syndromes? e.g. DVT, PE, RENAL VEIN THROMBOSIS

A

Hypercoagulable state due to

  1. Increased clotting factors produced by the liver as it goes into overdrive as there is low albumin
  2. Platelet abnormalities
80
Q

Why is there susceptibility to hyperlipidemia with nephrotic syndromes?

A

Increased cholesterol and triglycerides due to hepatic lipoprotein synthesis in response to low oncotic pressure due to low albumin.

81
Q

NEPHRITIC SYNDROME

82
Q

How does post-strepptococcal infection lead to nephritic syndrome? What is the treatment?

A

Bacterial antigen becomes trapped in the glomerulus leading to an act diffuse proliferative glomerulonephritis.
- Antibiotics and supportive treatment

83
Q

How does infective endocarditis lead to nephritic syndrome?

A

The deposition of circulating immune complexes in the kidney may produce interstitial nephritis or proliferative glomerulonephritis.

84
Q

How do you treat nephritic syndrome with SLE as cause?

A

Immunosuppression: steroids, cyclophosphamide, rituximab

85
Q

How does nephritic syndrome from systemic sclerosis present?

A
  • Ant nuclear antibody positive, AntiRo and Anti-la positive
  • severe hypertension
  • ONION SKIN changes on biopsy
  • Raynaud’s phenomenon
  • oesophageal dysmotility
86
Q

How does ANCA associated vasculitis lead to nephritic syndrome? What is the treatment?

A

Multisystem small vessel vasculitis attack small vessels in the kidney and eye.
Treatment; immunosuppression, steroids, cyclophosphamide, rituximab, plasma exchange.

87
Q

How does Good pastur’s disease lead to nephritic syndrome? What is the treatment?

A

Antibodies against the glomerular basement membrane.

Treatment: remove antibody via plasma exchange, immunosuppression: steroids, cyclophosphamide

88
Q

How does IgA neuropathy lead to nephritic syndrome? What is the treatment?

A

IgA deposition in mesangium of kidney and kidney gets attacked. Associated with tonsillitis and results in haematuria.
Treatment: BP control - ACEi, ARBs

89
Q

KIDNEY STONES

90
Q

Why are men more likely to develop retention?

A

Men have a greater voiding pressure due to them having a longer urethra

91
Q

Why are women more likely to develop incontinence?

A

Women have a shorter urethra with lower resistance and thus higher flow rates.

92
Q

Name some causes for hyperoxaluria

A
  1. High dietary intake: spinach, rhubarb, choclate and tea
  2. Low dietary Ca2+&raquo_space;>decreased binding of oxalate by ca2+»increase absorption and urinary excretion
  3. Increased intestinal resorption due to GI disease e.g. Crohn’s
93
Q

How can infections cause renal stones?

A

Mixed infective stones are composed of magnesium ammonium phosphate as well as calcium. These are often large and usually due to a UTI with organisms like Proteus mirabilis that hydrolyses urea»>ammonium hydroxide. The increased ammonium ions and the alkalinity both favour stone formation.

94
Q

How can dehydration cause renal stones?

A

Uric acid stones»

Increase in supersaturated urine

95
Q

UTI

96
Q

Give 5 host defence mechanisms against urinary tract infection.

A
  1. Antegrade flushing of urine- the forward flow of urine
  2. Tamm-Horsfall protein- antimicrobial properties
  3. GAG layer.
  4. Low urine pH and high osmolarity
  5. Commensal flora.
  6. Urinary IgA.
97
Q

Those with what blood group antigen tend to have recurrent UTI’s?

98
Q

Pathophysiology of pyelonephritis

A
  • Infection is mostly due to bacteria (primarily E.coli) from own patients bowel flora
  • Most common via accending transurethral route but can be via bloodstream or lymphatics.
99
Q

What are the 3 E.coli adhesive factors?

A
  1. P pilli : for urtheral ascent
  2. Aerobactin: for Fe acquisition
  3. Haemolysin: for pore formation
100
Q

CANCERS

101
Q

What is a cystoscopy?

A

Bladder endoscopy

102
Q

POLYCYSTIC KIDNEY DISEASE

103
Q

Name 6 different types of renal cysts

A
  1. Simple cysts
  2. Polycystic (dominant or recessive)
  3. Hydronephrosis (ureter blocked> kidney dilates)
  4. Dysplasia - not formed properly
  5. Medullary sponge - dilation of collecting ducts
  6. Acquired cysts: medullary uraemic, dialysis cystic, associated with CKD
104
Q

What drug can cause renal cysts?

A

Lithium (used to treat depression)

105
Q

What syndrome can cause renal cysts?

A

Tuberous sclerosis

106
Q

Pathophysiology of ADPKD

A
  • PKD 1 encodes for polycystin 1: responsible for renal tubular and vascular development
  • PKD 2 encodes for polycystin 2: type of calcium ion channel
  • Polycystin complex occurs in cilia and is responsible for sensing flow in the tubule.
  • Disruption of this polycystin pathway results in reduced cytoplasmic Ca2+
  • In the principal cells of the collecting duct causes defective ciliary signalling and disorientated cell division leading to cyst formation.
  • Mechanical compression, apoptosis of healthy tissue and reactive fibrosis= progressive loss of renal function
    RENAL FUNCTION DECLINE DEPENDANT ON SIZE AND GROWTH OF CYSTS.
107
Q

What are the two types of cells in the collecting duct? The function of each?

A
  1. Principle cells
  2. Intercalated cells (A+ B)
    Principal cells are the main Na+ reabsorbing cells and the site of action of aldosterone, K+-sparing diuretics, and spironolactone.
    Type A intercalated cells mediate acid secretion and bicarbonate reabsorption.
    Type B intercalated cells mediate bicarbonate secretion and acid reabsorption.
108
Q

What are the diagnostic criteria for at-risk individuals for ADPKD?

A

15-39 y.o. ≥3 cysts (unilateral/bilateral)
40-59 y.o ≥2 cysts (each kidney)
≥60 y.o. ≥4 cysts (each kidney)

109
Q

Give some indications for genetic testing:

A
  1. Individual older case with no FHx
  2. Atypical cystic disease
  3. Very early-onset <2yrs
  4. Prenatal/Pre-implantation genetic diagnosis
  5. To facilitate life choices/ reproductive decisions
  6. Potential living-related kidney donor
110
Q

RENAL TUBULAR ACIDOSIS

111
Q

What is renal tubular acidosis?

A

Group of conditions causing metabolic acidosis due to pathology in kidney tubules.

112
Q

What is type 1 renal tubular acidosis? Causes of this?

A

Pathology in the distal tubules. The inability of distal tubules to excrete hydrogen ions. Causes:

  • Genetic mutations
  • autoimmune disorders
  • hyperparathyroidism
  • chronic UTI’s
113
Q

What is type 2 renal tubular acidosis?

A

Pathology in the proximal tubules

114
Q

What is type 3 renal tubular acidosis?

A

A mix of distal and proximal tubule pathology

115
Q

What is type 4 renal tubular acidosis?

A

Reduced aldosterone&raquo_space;>hyperkalaemia

116
Q

What investigations do you perform for renal tubular acidosis?

A
  1. Blood gases (hypokaleamia. metabolic acidosis)
  2. U+E
  3. Urine pH (high>6)
117
Q

What does type 1 renal tubular acidosis present with and what is the treatment?

A

Hyperventilation, muscle weakness, cardiac arrhythmias, bone pain.
Oral bicarbonate

118
Q

What does type 2 renal tubular acidosis present with and what is the treatment?

A

Polyuria, polydipsia, osteomalacia/rickets

Oral bicarbonate and vit D supplements

119
Q

What is the aetiology of type 4 RTA?

A

Medical: Adrenal insufficiency (Addison’s), SLE
Pharmacological: ACEi, spironolactone, NSAID’s, beta-blockers

120
Q

What does type 4 renal tubular acidosis present with and what is the treatment?

A

Urinary pH: <5.4
Bloods: hyperkalaemia
Fludrocortisone

121
Q

EPIDIDYMAL CYST

122
Q

A testicular lump is?

A

CANCER until proven otherwise

123
Q

If you cannot get above the lump?

A

Iguinoscrotal hernia or proximally extending hydrocele

124
Q

If the lump can be separated and is cystic?

A

Epididymal cyst

125
Q

If the lump can be separated and is solid?

A

Epididymitis or varicocele

126
Q

If the lump is testicular and cystic?

127
Q

If the lump is testicular and solid?

A

Tumour, haematocele

128
Q

HYDROCELE

129
Q

Pathophysiology of hydrocele

A

Overproduction of fluid in the tune vaginalis or the processus vaginalis fails to close, allowing peritoneal fluid to communicate freely with the scrotal portion.

130
Q

VARICOCELE

131
Q

WHY IS IT MORE COMMON ON THE LEFT SIDE?

A
  1. angle at which L testicular vein enters L renal vein
  2. lack of effective valves between L testicular and L renal vein
  3. increased reflux from compression of renal vein
132
Q

What is a sign of LEFT renal cancer?

A

A sudden onset LEFT varicocele in an older man that doesn’t disappear when lying flat can be a sign of cancer. This is due to the compression of the left testicular vein by renal cell carcinoma.

133
Q

What is an direct inguinal hernia?

A

A portion of the small intestine pushes through an opening/weakness in tissue separating the abdomen and the groin. Direct is when it comes through the muscle wall.

134
Q

What is an indirect inguinal hernia?

A

A portion of the small intestine pushes through an opening/ weakness in tissue separating the abdomen and the groin. Indirect is when it comes through the inguinal ring.

135
Q

How to differentiate an inguinal hernia?

A

CAN’T GET ABOVE THE TESTICLES.

136
Q

Epididymitis

A

inflammation of the epididymis

137
Q

Orchitis

A

inflammation of testis

138
Q

What is the usual cause of epididymal-orchitis?

A

under 35 = STI e.g. chlamydia trachomatis, nesseria gonorrhoae
over 35 = UTI e.g. KEEPS

139
Q

What are the signs and symptoms of epididymal-orchitis?

A
  1. Acute/subacute onset
  2. Unilateral scrotal pain and swelling.
  3. Urethritis and discharge
  4. Dysuria
  5. Sweats and fever
  6. Tenderness and palpable swelling
140
Q

What investigations would you carry out for epididymal-orchitis?

A 
1. Nucleic Acid Amplication Test  (NAAT)
female vaginal swab 
maid first void urine 
2. MSU and dipstick 
3. Ultrasound for abscesses
141
Q

Treatment for epididymal-orchitis?

A

Abx:
<35y.o = doxycycline + ceftriazone (if gonorrhoea suspected)
>35 y.o. = CIPROFLOXACIN/OFLOXACIN
Analgesia

142
Q

URINARY INCONTINENCE

143
Q

What is urinary incontinence?

A

Loss of control of voiding in the bladder leading to the unintentional and involuntary passage of urine.

144
Q

What does a spastic spinal cord injury lead to?

A

Supra-conal lesion»Reflexes work but are not controlled by the brain.

  • Loss of co-ordination and completion of voiding
  • REFLEX BLADDER contractions
  • Detrusor sphincter dyssynergia
  • poorly sustained bladder contraction
  • involuntary urination
  • urge incontinence
145
Q

What does a flaccid spinal cord injury lead to?

A

Conus lesion&raquo_space;>decentralised bladder

  • Reflex bladder contraction is lost, bladder is AREFLEX
  • Bladder fills until it overflows
  • Overflow incontinence- stress
  • Loss of receptive relaxation
  • Consider permanent catheristaion.
146
Q

The sepsis 6

A
  1. Give high flow oxygen via a non-breathe bag
  2. Take blood cultures and consider source control
  3. IV ABx
  4. IV fluid resuscitation
  5. Check lactate- marker for systemic tissue hypoperfusion and it reflects cellular dysfunction
  6. Monitor urine output and consider catheterization
    ALL WITHIN AN HOUR

Phase 2A extra (7 decks)

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