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CMT > Renal Pathophys > Flashcards

Renal Pathophys Flashcards

1
Q

Potassium

Secretion/Excretion

A
  • In kidneys, the majority of filtered K+ is resorbed in the proximal tubular system
  • Selective secretion or absorption in the distal tubule determines net K+ (limit of renal K+ excretion 10 mEq/L)
  • Excretion affected by circulating Aldosterone, cellular and extracellular K+, tubular urine flow rates, & acid-base disturbances

Misc Info
* 98% of K+ is intracellular
* 95% is excreted in urine; rest is swewat/feces

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2
Q

Potassium

Function

A

Na+/K+ ATPase
* nerve transmission
* skeletal msk contraction
* cardiac msk function
* renal/fluid ion balance

K+ Channels
* nerve action potentials

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3
Q

Potassium

Tx Hypokalemia (when to use what)

A
  • Orally: preferred; use in normal renal function; do not exceed 40 mEq/hr
  • IV: if emergent; do not exceed 10 mEq/hr; repeat as often as necessary; EKG monitor (mandatory if rate >10 mEq/hr); avoid dextrose solutions (will drop K level)
  • correct hypokalemia + hypocalcemia together
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4
Q

Chloride

normal levels

A

98-110 mEq/L

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5
Q

Calcium

normal value + how to correct

A
  • normal: 8.5-10.5 mEq/L
  • must correct for albumin when pt is hypoalbuminemic because 40% is bound to albumin
  • corrected: serum Ca2+ = measure Ca 2+ + [0.8 x (normal albumin-measured albumin)]
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6
Q

Calcium

function of calcium

A
  • Neural signaling
  • Bone mineralization
  • Cardiac function
  • Skeletal muscle contraction
  • Digestive system function
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7
Q

Calcium

factors affecting resorption

A

PTH or metabolic alkalosis

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8
Q

Calcium

pathophys of calcium

A
  • Stimulates osteoclasts to break down bone – releasing calcium and phosphorus
  • Increases reabsorption of calcium by kidneys
  • Blocks reabsorption of phosphate by kidneys, leading to urinary phosphate loss.
  • Increases conversion of inactive to active 1,25 vitamin D (which then increases calcium absorption from gut)
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9
Q

Hypocalcemia

Trousseau vs Chvostek

A
  • Trousseau: Carpal spasm elicited by inflation of BP cuff to 20 mmHg above systolic pressure for 3 min
  • Chvostek: Twitching of circumoral muscles in response to tapping facial nerve anterior to ear
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10
Q

Calcium

how does half or full NS help hypercalcemia

A
  • Enhances urinary calcium excretion
  • Saline diuresis lead to hypokalemia, hypomagnesemia, or other electrolyte imbalance
  • CAUTION: avoid fluid overload
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11
Q

Magnesium

generally describe

A
  • 2nd most abundant cation of the intracellular fluid
  • Mg++ is tightly regulated by the gut, kidney, and bone.

Function
* Activates enzymes
* ATP function in combination with phosphate
* Signal transduction pathways
* Nerve transmission

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12
Q

Phosphorus

generally describe

A
  • Normal 3 to 4.5 mg/dL
  • Total body content: 85% in bone, 14% intracellular, and 1% extracellular
  • Daily intake is 800 to 1500 mg
  • Present in many foods: dairy products, meats, grains

Kidney secretes phosphorus
* Most filtered at the glomerulus
* PTH increases renal phosphate excretion
* Vitamin D enhances intestinal phosphate absorption

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13
Q

Phosphorus

pseudohyperphosphatemia

A

Pseudohyperphosphatemia may occur in hemolytic specimens or hyperglobulinemic states (ie, multiple myeloma)

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14
Q

functions of the kidney

A
  • Regulation of ionic composition (Sodium, potassium, calcium, chloride, phosphate)
  • Regulation of blood pH, osmolarity, and glucose
  • Regulation of blood volume (Conserving or eliminating water)
  • Regulation of blood pressure (Secreting renin)
  • Release of erythropoietin & calcitriol
  • Excretion of wastes (Nitrogenous waste products (ammonia, uric acid, urea, creatinine, and amino acids), excess quantities of salts and water
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15
Q

Kidneys General Anatomy/Physio

describe erythropoietin and calcitriol

A
  • Erythropoietin: essential hormone secreted by the kidneys for red blood cell production in the none marrow
  • Calcitriol: active form of vitamin D; also known as 1,25-dihydroxycholecalciferol
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16
Q

Kidneys General Anatomy/Physio

internal anatomy of kidney

A

Renal parenchyma
* Glandular tissue that forms urine
* Divided into 2 sections

Renal cortex
* Superficial layer of the kidney; measures ~1 cm
* Extension of the cortex known as renal columns

Renal medulla
* Inner section consisting of 6-18 conical renal pyramids

Renal pyramid
* Blunt end called the papilla that is nestled in a cup called a minor calyx for urine collection

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17
Q

Kidneys General Anatomy/Physio

nephrons

A
  • Functional unit of the kidney
  • ~1.2 million per kidney
  • Composed of: Blood vessels, renal corpuscle, and renal tubule

Cortical nephrons
* 70-80% of the nephrons
* Located close to the kidney surface

Juxtamedullary nephrons
* 20-30% of the nephrons
* Located close to the medulla

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18
Q

Kidneys General Anatomy/Physio

major function of the kidney

A
  • Filter blood plasma and separate wastes from the useful chemicals
  • Eliminates the wastes in urine while returning the useful chemicals to the bloodstream
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19
Q

Kidneys General Anatomy/Physio

Renal Corpuscle

A
  • Component of each nephron
  • Site where blood filtration begins (Passive process by high hydrostatic pressure of the glomerular capillaries)
  • Consists of: Glomerulus (cluster of capillaries), Bowman’s capsule, Two-layered capsule that encloses the glomerulus

Blood Flow
* Blood flows into the glomerulus via the afferent arterioles → water and solutes pass through the capillary endothelium, through the basement membrane, and through the epithelium → Bowman’s space → renal tubule
* Remaining blood leaves the glomerulus through efferent arterioles

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20
Q

Kidneys General Anatomy/Physio

Glomerular Filtration Rate (GFR)

A
  • The volume of fluid filtered by the kidneys in a minute
  • Measures kidney function

Dependent upon:
* The net filtration pressure (Vasodilation of the afferent arterioles mediated by prostaglandins; Vasoconstriction of the efferent arterioles mediated by angiotensin II)
* Available surface area for filtration
* Filtration membrane permeability

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21
Q

Kidneys General Anatomy/Physio

Renin-Angiotensin-Aldosterone (RAAS) system

A
  1. angiotensinogen (liver)
  2. renin (kidney)- converts-
  3. angiotensin I
  4. antiongensin converting enzyme (ACE) - (lungs/kidney) - converts-
  5. angiotensin II
  6. systemic effects

plays central role in regulation of renal blood flow

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22
Q

Kidneys General Anatomy/Physio

RAAS end system impacts

A
  • vasoconstricts the glomerular arterioles; greater effect on the efferent arterioles than the afferent arterioles → increased glomerular filtration pressure
  • Increased circulating volume from the affects of aldosterone → increased blood pressure and renal perfusion
  • stimulates the release of antidiuretic hormone (ADH), which will reabsorb water from the collecting ducts → increased circulating blood volume and renal perfusion
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23
Q

Kidneys General Anatomy/Physio

Renal Tubule

A
  • Duct that leads away from the glomerular capsule
  • Each has a unique absorptive properties

Divided into 4 regions:
* Proximal convoluted tubule (PCT)
* Nephron loop
* Distal convoluted tubule (DCT)
* Collecting duct

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24
Q

AKI

epidemiology

A
  • 7% hosp patients
  • 2/3 of ICU pts (50-70% mortality if associated w/ sepsis or multi-organ failure)
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25
Q
A
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26
Q

AKI

pre-renal causes

A
  • Most common type of AKI (70% of community-acquired cases)

Caused by decreased renal perfusion
* Reduced circulating volume (GI losses, blood loss, diuretic use, osmotic diuresis – DKA, insensible loss – burns)
* Reduced cardiac output (heart failure)
* Systemic vasodilation (septic shock)
* Medications
* ACE inhibitors, ARBs, NSAIDs
* Obstruction of the renal artery (thrombosis/embolus, stenosis, or aneurysm)

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27
Q

AKI

NSAID vs ACE/ARB impacts on kidneys

A

NSAIDs
* Vasodilation of the afferent arterioles mediated by prostaglandins
* NSAIDs block the production of prostaglandins → vasoconstriction and possible AKI

ACE/ARB
* Vasoconstriction of the efferent arterioles mediated by angiotensin II
* ACEi/ARBs block the effects of angiotensin II (vasoconstriction) → vasodilation of the efferent arterioles (renal protective)
* In patients with renal artery stenosis, the introduction of an ACEi/ARBs can lead to a drop in glomerular filtration pressure

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28
Q

AKI

Intrinsic/Intra-renal causes

A
  • Caused by direct damage to the glomeruli and/or tubulointerstitial structures

Acute tubularnecrosis(ATN)
* Damage to the tubular cells
* Caused by a lack of blood flow to the kidneys and nephrotoxic agents

Acute interstitial nephritis
* Inflammatory cell infiltration into the kidney interstitium
* Caused by medications,infections, orautoimmune diseases

Vascular disease
* Atherosclerosis and vasculitis

Glomerular disease
* Glomerulonephritis (presents withhematuria)
* nephrotic syndrome(presents withproteinuria)

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29
Q

AKI

nephrotoxic agents

A
  • aminoglycosides
  • vancomycin
  • cisplatin
  • heavy metals (lead, mercury)
  • ethylene glycol (anti-freeze)
  • radiocontrast
  • lithium
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30
Q
A
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31
Q

AKI

post-renal causes

A
  • Caused by inadequate drainage of urine distal to the kidneys (obstruction) leading to back pressure on the kidneys and hydronephrosis
  • May occur at any point in its course from therenal pelvisto theurethra

Causes of obstruction
* Urinary calculi
* Benign prostatichyperplasia (BPH) or prostate cancer
* Bladder outlet obstruction
* Urethral stricture
* Gynecologic tumors (ovarian cancer, uterinefibroids,cervical cancer)

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32
Q

AKI

effects of AKI on electrolytes & acid-base balance

A

Hyperkalemia
* Due to decreased renal excretion ofpotassium
* Increases theprobability ofcardiac arrhythmias

Hyperphosphatemia
* Due to decreased renal excretion ofphosphate

Metabolic acidosis
* Inability of thekidneysto excreteacids
* Exacerbateshyperkalemia
* Increases theprobabilityofcardiac arrhythmias

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33
Q

Rhabdo

causes

traumatic, exertional, non-exertional

A

Traumatic (msk compression)
* Crush injuries
* Victims of prolonged restraint, torture, or physical abuse
* Surgical procedure with prolonged muscle compression
* Acute lower-limb compartment syndrome
* High-voltage electrical injury

Non-Traumatic, Exertional
* marked physical exertion when 1+ risk factors is present: sickle cell trait, physically untrained, hot/humid conditions, impaired heat loss (ex: anti-cholinergic meds, heavy football equiment)
* pathologic hyperkinetic states: grand mal seizures, delirium tremens (severe type of EtOH withdrawal), psychotic agitation, amphetamine OD

Non-Traumatic, Non-Exertional
* Prolonged immobilization
* Alcohol use
* Drug use: Illicit (heroin, cocaine, LSD, methadone) or Prescription (statins, colchicine, daptomycin)
* Toxins: Snake venom, mushroom poisoning, carbon monoxide
* Infections: Viral (influenza A & B, coxsackievirus)
* Inflammatory myopathies (dermatomyositis)
* Electrolyte abnormalities: Hypokalemia or Hypophosphatemia

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34
Q

Rhabdo

pathogenesis

A
  • Muscle injury
  • Influx of extracellular sodium and calcium into the myocytes; water follows sodium distorting the integrity of the intracellular space
  • ↑ intracellular calcium causes a sustained myofibril contraction → ATP depletion within these cells
  • Activation of lipases and proteases → damage of the myocyte cellular membrane
  • Release of intracellular components (creatine kinase (CK), myoglobin, potassium, phosphate) that enter the bloodstream
  • Myoglobinuria and electrolyte abnormalities cause end-organ complications (AKI most common systemic complication)
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35
Q

Rhabdo

electrolyte balance

A

Intracellular fluid
* Potassium (K⁺) – main cation
* Magnesium (Mg2⁺)
* Proteins
* Phosphates (HPO₄²-/H₂PO₄-) – main anion
* Electrically balance the intracellular cations along with the negatively chargedproteins
* MP3 (Mg, potassium, protein, phosphate) Inside

Extracellular fluid
* Sodium (Na⁺) – main cation
* Controls ECF volume and water distribution in the body – water follows sodium
* Calcium (Ca²⁺)
* Chloride (Cl-) and Bicarbonate (HCO₃-):Chloride is the most abundant anion in the ECF
* Anions balance the extracellular cations

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36
Q

Horseshoe Kidney

anat/phys

A
  • renal fusion when a portion of one kidney is fused to the other due to abnormal migration of kidneys; horseshoe most commonly is each pole fused together
  • isthmus lies in the mid-line or sometimes slightly lateral to the mid-line and can be composed of renal parenchyma or just fibrous tissue, but the renal collecting systems remain separate

Anatomy
* fusion occurs before the kidneys ascend from the pelvis to their normal dorsolumbar position (5th-9th wks gestation)
* fusion abnormalities found in lower lumbar vertebral level (L4/5)
* blood supply variable

37
Q

Wilms Tumor

epidemiology

A
  • 5% cancers in children under age 15
  • second most common abd tumor
  • some occur in setting of associated malformations or syndromes
  • bilateral tumors more common in younger kids
  • males dx earlier than females
  • occurs most commonly between ages 2-5
38
Q

Cryptorchidism- technique for assessing location

A
  • Exam should be focused on whether testes can be palpated in the scrotum or inguinal canal, appearance of the genitalia, and any midline defects.
  • Will need two hands to perform the exam.
  • One hand milks the testes from the deep inguinal ring to the scrotum.
  • The second hand lies over the scrotum to hold the testis.
  • If the testis retracts back to the inguinal canal, it is likely undescended testicle. If the testis stays in the scrotal sack, then likely it will be a normal testicle.
  • Squatting position for older children or in a warm bath is helpful for examination.
39
Q

Bladder Cancer

describe cystoscopy + bx

A
  • Cystoscopy is performed in the OR with local anesthesia or in the office with lidocaine injected into the urethra to look for a bladder tumor.
  • If a bladder tumor is noted, then patient is scheduled back in the OR with either general or regional anesthesia for transurethral resection of the bladder tumor (TURBT)
40
Q

Bladder Cancer

describe intravesical therapy

A
  • Intravesical therapy is using chemotherapy or immunotherapy that is delivered directly into the bladder by a urethral catheter to help reduce reoccurrence after a complete transurethral resection.
  • Agents are given weekly for 6-12 weeks.
  • Recommend to patients they keep the liquid in their bladder for 2 hours if possible.
  • Can be given in the urologist’s office.
  • Most effective agent to reduce disease progression is bacillus Calmette-Guerin (BCG).
  • Side effects include irritative voiding symptoms and hemorrhagic cystitis.
41
Q

Bladder Cancer

Chemo

A
  • 15% of patients with newly diagnosed bladder cancer will have metastases.
  • Metastases will develop up to 40% of patients within 2 years of having their bladder removed.
  • Cisplatin-based combination therapy is the preferred approach for them, so offering adjuvant chemotherapy is helpful for those with high risk for reoccurrence.
  • Neoadjuvant chemotherapy appears to benefit all patients with muscle-invasive cancer prior to having a cystectomy performed.
  • Chemotherapy is considered for those with bulky lesions or regional metastases.
42
Q

Bladder Cancer

Radiation

A

External Beam Radiation
* Delivered in fractions over a 6–8-week period.
* 10-15% of patients will develop bladder, bowel, or rectal complications.
* 30-70% of patients will have reoccurrence with radiotherapy alone.
* Systemic chemotherapy is offered in conjunction with radiation to some patients.

43
Q

Bladder Cancer

Immunotherapy

A
  • Immunotherapy consists of drugs called Anti-PDL-1 inhibitors.
  • These checkpoint inhibitors are approved as second line therapy for metastatic urothelial cancer by the FDA after the patient has received platinum-based chemotherapy.
  • Immune checkpoints are molecules on certain immune cells that need to be activated or inactivated to start an immune response.
  • Checkpoint inhibitors don’t work directly on the tumor but allows the immune response that has only started, to progress to full force.
  • PD-1 is a checkpoint protein on T cells. Normally it is an “off switch” that helps keep the T cells from attacking the other cells in the body.
  • When PD-1 (a protein on normal and cancer cells) binds to PD-L1, it tells the T cells to leave that particular cell alone.
  • Some cancer cells have large amounts of PD-L1, which helps them hide from an immune attack.
  • Monoclonal antibodies that target either PD-1 or PD-L1 can block the binding and boost the immune response against cancer cells.
44
Q

Bladder Cancer

Immunotherapy- PD-L1 inhibitors & PD-1 inhibitors

A

Examples of PD-L1 inhibitors include:
* Durvalumab (Imfinzi)
* Avelumab (Bavencio)
* Atezolizaumab (Tecentriq)

Examples of PD-1 inhibitors include:
* Nivolumab (Opdivo)
* Pembrolizumab (Keytruda)

45
Q

Bladder Cancer

prognosis

A
  • The frequency and progression are correlated with grade.
  • Progression is more common with poorly differentiated lesions and carcinoma in situ that is associated with papillary bladder cancers.
  • At initial presentation, 50-80% of bladder cancers are superficial that include stage Ta, Tis, T1.
  • When properly treated, survival rate is excellent at 81%.
  • 5-year survival of patients with T2 and T3 diseases are 50-75% after radical cystectomy.
  • Long term survival is rare for patients with metastatic disease at time of presentation.
46
Q

transient causes urinary incontinence

A
  • Delirium
  • Infection
  • Atrophic urethritis and vaginitis
  • Pharmaceuticals
  • Psychological Factors
  • Excess Urinary Output
  • Restricted Mobility
  • Stool Impaction

DIAPPERS

47
Q

established causes urinary incontinence

A
  • Detrusor Overactivity/Urge Incontinence
  • Urethral Incompetence/Stress Incontinence
  • Overflow Incompetence
48
Q

Urinary Incontinence

describe detrustor overactivity/urge incontinence

A
  • Detrusor overactivity refers to uncontrolled bladder contractions that cause leakage.
  • It’s the most common cause of incontinence in older adults, accounting for two-thirds of the cases.
  • In women, they will have urinary leakage after an intense urge to urinate that cannot wait.
  • Men have similar symptoms but usually their detrusor overactivity coincides with urethral obstruction from benign prostate hyperplasia.
  • Overactive bladder is characterized by frequency, urgency, and nocturia.
  • Can present with or without urge incontinence.
49
Q

Urinary Incontinence

patho of urge incontinence

A
  • The underlying mechanism of urge incontinence is bladder overactivity, so uninhibited bladder contractions occur during the filling and storage phase.
  • Most women will not find any type of identifiable pathology.
  • Some patients as they get older, also have impaired bladder contractility.
  • This increases the risk of urinary retention by reducing the intravesical bladder pressure in overcoming bladder outlet pressure during bladder contractions, which is now thought to be a function of bladder underactivity.
50
Q

Urinary Incontinence

pelvic exam for detrustor overactivity/urge incontinence

A

Pelvic examination:
* To test for urge incontinence, have the patient relax her perineum and cough vigorously while standing with a full bladder. The patient may also lay on the table and perform Valsalva test (bearing down as if trying to have a bowel movement).
* Delayed leakage of several seconds or persistent leakage suggests that the problem is caused by uninhibited bladder contraction induced by coughing.

51
Q

Urinary Incontinence

detrustor overactivity/urge incontinence- in who should you add on an alpha blocker

A
  • men with BPH and detrusor overactivity
  • PVR < 150 mL
52
Q

Urinary Incontinence

describe urethral incompetence/stress incontinence

A
  • Second most common case of established urinary incontinence in older women.
  • Stress incontinence is most commonly seen in men after a radical prostatectomy.
  • It is characterized by instantaneous leakage of urine in response to an increase in intra-abdominal pressure.
  • This can occur along with detrusor overactivity and have a “mixed incontinence.”
  • Typically has urinary loss with laughing, coughing, or lifting heavy objects.
53
Q

Urinary Incontinence

pathophys of urethral incompetence/stress incontinence

A
  • The primary issue of stress incontinence is urethral underactivity, related to either decreased tone of the internal urethral sphincter or hypermobility of the bladder neck.
  • Stress incontinence occurs with elevated intra-abdominal pressure, which causes a sudden increase in the bladder pressure. (Normally these changes are counteracted by contractions of the internal urethral sphincter. Stress incontinence occurs when the bladder pressure is higher than that of the urethra.)
  • Hypermobility of the bladder refers to displacement of the bladder neck and urethra during increases of intra-abdominal pressure. (Normally this results in the urethra compressed against the muscles of the anterior vaginal wall, which provides support for both the bladder neck and urethra. If the muscles are weak, they can’t provide this support, which displaces them both so incomplete urethral closure and leakage of small amounts of urine occur.)
  • Stress incontinence is commonly related to vaginal deliveries and hormonal changes associated with menopause in women.
54
Q

Urinary Incontinence

describe overflow incontinence

A
  • This occurs when urinary retention leads to bladder distention and overflow of urine from the urethra.
  • Urethral obstruction (due to prostatic enlargement, urethral stricture, bladder neck contracture, or prostate cancer) is a common cause of established incontinence in older men but rare in older women.
55
Q

Urinary Incontinence

pathophys of overflow incontinence

A
  • Overflow incontinence is related to bladder underactivity and/or outflow obstruction.
  • When the bladder is filled to capacity, the bladder cannot empty due to poor contractility or obstruction around the urethral sphincter.
56
Q

Key Points CKD

A
  • abnormal kidney function > 3 mo (GFR < 60 mL/min or proteinuria, or albuminuria)
  • primary causes are DM, HTN, ASCVD
  • independent risk factor for CAD
  • Proteinuric CKD has worse prognosis
57
Q

CKD

meds with dose adjustments

A
  • Augmentin : avoid 875mg with CrCl< 30; use 250-500 mg
  • Amoxicillin: 250-500 mg po q 12 if CrCl< 30
  • Clarithromycin: reduce dose by 50% if CrCl< 30
  • Ciprofloxacin: reduce 500 mg q 24 hours CrCl < 30
  • Levaquin: reduce dose to q 48 hours CrCl < 50
  • Bactrim: reduce usually dose 50% CrCl < 30
  • Nitrofurantoin: contraindicated GFR < 60?
  • Metronidazole: adjust CrCl< 10
  • Cephalexin
  • Tamiflu
  • Allopurinol: reduce 50 mg daily CrCl < 60
  • Colchicine: avoid GFR , 30
  • Indomethacin: avoid GFR < 60
  • Meloxicam: reduce CrCl < 20
  • Ibuprofen: avoid GFR < 60
  • Naproxen: avoid GFR < 30
  • Percocet: reduce dose q 12 if GFR < 30
58
Q

CKD

no-no meds

A
  • NSAIDS, COX-2
  • Proton pump inhibitors ( in CKD 4 or later)
  • Magnesium-containing antacids (tums, Rolaids, Gaviscon, Alka-seltzer)
  • IV contrast dye
  • aminoglycoside, vancomycin, trimethoprim/sulfamethoxazole
  • Digoxin
  • Over the counter: magnesium citrate!!!
  • when GFR < 30 caution with most medications
59
Q

CKD

screenings for stage I-IV

A
  • Yearly BMP, UACR, Lipids
  • BP < 120/80 ( ace/arb); NA < 1.5 g daily
  • Statin: moderate intensity pts > 50 yoa GFR < 60ml/min
  • Low dose asa if low bleeding risk?
  • Current vaccinations
  • Remember risk for ASCVD!!!
60
Q

additional screenings for stages III and IV

A
  • BMP
  • UACR
  • Lipids
  • PTH
  • Ca/Vit D
  • CBC
  • Phosphorus
61
Q

ESRD

Hemodialysis access Types

A
  • AV Graft: 2-4 wks to develop; increased risk clot/infection
  • CVC: immediate use; usually into internal jugular, subclavian, or femoral; temporary use only, don’t allow for large volume
  • AV Fistula: 2-6 mo to form; lower risk of clot/infection; conects an artery to a vein; lasts for years
62
Q

Hemodialysis

generally describe

A
  • Filtration of patient’s blood with a dialyzer; continuous or intermittent
  • Corrects imbalances of electrolytes, fluids, toxins, and waste
  • Must leave home 3 x a week
  • Restricted diet
  • Can feel “ yuck “ after
  • In general, refer patients for access before GFR < 15
63
Q

Hemodialysis

describe AV fistulas

A
  • Av fistula usually takes 2-6 months to form
  • Less risk of clots or infection and last for years
  • Connect the artery to the vein
  • Surgeon may order vessel mapping to determine size and quality of veins and flow
  • Affected limb care includes no venipuncture/bp
64
Q
A
65
Q

describe AV Grafts

A
  • If pt has small or weak veins that will not develop into fistula may use a synthetic graft or tube to create connection
  • Usually needs 2-4 weeks to develop
  • +/- bruit or thrill
  • Increased risk clotting and infection; do not often last as long as AV fistula
  • Limb care includes no venipuncture, BP, heavy lifting
66
Q

CVC: generally describe

A
  • Flexible, hollow tube inserted into large vein (Internal jugular, subclavian, femoral)
  • Usually a means for temporary dialysis
  • High infection rate
  • Do not allow for large volume – can affect treatment
  • Veins can develop stenosis or clot
  • Usually changed every 4 weeks
  • Swimming/bathing not recommended
67
Q

Peritoneal Dialysis

A
  • Dialysis via the peritoneum
  • Does not require vascular access
  • Less stressful on the patient- decreased side effects, can be done at home
  • less effective than hemodialysis
  • Protein loss and increased risk for peritonitis
  • Requires intra-abdominal catheter- risk infections and adhesions
67
Q

Polycystic Kidney Disease (PKD)

role of polycystin proteins

A

Polycystin proteins allow calcium influx, which activates pathways in the cell that inhibit cell proliferation; mutations cause cells to proliferate abnormally and start to express proteins that cause water to be transported into the lumen of the cyst, which makes them get larger and larger, compressing the surrounding tissue more and more

68
Q

PKD

autosomal dominant vs recessive PKD

A

DOMINANT
* located on non-sex chromosome
* s/sx appear between 30-40 yrs

RECCESSIVE
* s/sx appear shortly after birth or into adolescence

69
Q

Nephrolithiasis

  1. which stones are radiopaque?
  2. which stones are infectious?
  3. which stones are genetic?
A
  • all are except uric acid stones
  • struvite are infection stones
  • cystine stones are genetic (autosomal recessive defect in sodium-dibasic amino acid cotransporter
70
Q

nephrolithiasis

staghorn calculi

A
  • AKA coral calculi
  • usually type of struvite stone
  • branched stones that occupy large portion of collecting system (renal pelvis + calyces)
  • can damage the kidney and/or lead to life threatening urosepsis
71
Q

medical conditions associated w/ stones

A
  • Primary hyperparathyroidism (high calcium levels)
  • Gout (high uric acid)
  • Hypertension
  • Diabetes mellitus
  • Obesity
  • Inflammatory bowel disease (IBD)
  • Short gut syndrome
  • Gastrointestinal bypass surgery
  • Urinary tract infections (chronic upper urinary tract)
72
Q

Nephrolithiasis

site of obstruction + location of pain

A
  • Upper ureter or renal pelvis: flank pain w/ CVA tenderness
  • Lower ureter: radiates to labium or ipsilateral testicle
73
Q

Nephrolithiasis

sites of obstruction

A

Ureteropelvic junction(UPJ)
* Junction of therenal pelvisand ureter

Ureter at thepelvic inlet
* Site of ureteral crossing of the iliac vessels

Ureterovesical junction (UVJ)
* Junction of the ureter andurinary bladder

74
Q

patho phys of urine

A
  • Made by the kidneys by filtering wastes and extra water from the blood

1-2 L of urine is produced daily
* Polyuria: excessive urine output; > 2L/day
* Oliguria: output of < 500 mL/day
* Anuria: output of 0-100 mL/day

Appearance
* Yellow color due to urochrome, a pigment from the breakdown of hemoglobin
* Variation of color due disease states, hydration status, foods eaten, and medications
* Pyuria: pus in the urine; cloudy due to infection
* Hematuria: blood in the urine; can be gross or microscopic

75
Q

what can turn the urine orange? flourescent yellow?

A
  • orange: azo/pyridium
  • fluorescent yellow: excess vitamin B
76
Q

Normal Urine

A

Odor
* Affected by the foods we eat
* “fruity” odor: acetone in diabetic patients
* “foul/strong” odor: may indicate acute UTI

Chemical composition
* 95% water and 5% solutes (urea, sodium, potassium, chloride)
* Glucose, free hemoglobin, albumin, ketones, and bile pigments in urine are indicators of disease

pH
* Ranges from 4.5-8.2, but is normally mildly acidic at 6.0

Specific gravity
* Ratio of the density of a substance to the density of distilled water
* Range from 1.001 (dilute) to 1.035 (concentrated)

77
Q

lower UTI vs upper UTI

A
  • lower: urethritis, prostatitis, cystitis
  • upper: pyelonephritis
78
Q

how does the urinary tract maintain sterility?

A
  • Urine acidity
  • High urea concentration
  • Emptying of the bladder (micturition)
  • Ureterovesical and urethral sphincters
  • Mucous secretions: Urethra in ♀, Prostate in ♂
  • Protective uroepithelial immune response
  • Secretion of uromodulin from the kidneys
79
Q

Glomerular Diseases

function of glomeruli

A
  • Blood enters the glomerulus. The glomerulus filters the blood and decides what to resorb and pass thru kidney ( ions, H20, protein, urea, minerals, vitamins, drugs) and what to not absorb and kick out into the urine.
  • A normal glomerulus forms a tight barrier which prevents passage/leaking of blood and or protein into the urinary filtrate. When glomerulus is damaged or inflamed the barrier is compromised which allows passage of blood and or protein thru the barrier. This is the earliest sign of glomerular lesion- if left untreated and it progresses eventually the GFR will decline.
80
Q

Glomerular Disease

3 barriers that help filter

A

Fenestrated endothelium
* Endothelial cells that look like honeycombs with large pores (70-90 nm)
* Small enough to exclude blood cells from the filtrate

Glomerular basement membrane (GBM)
* Size- and charge-selective barrier to the passage of macromolecules from the plasma
* Excludes any molecule larger than 8 nm
* Prevents negatively charged particles from passing
* Albumin is a ~7 nm protein and negatively charged → repelled by the basement membrane

Podocytes of the epithelium
* ~30 nm wide and negatively charged

81
Q

Glomerular Disease

proteinuria

A
  • Proteinuria if a marker of renal parenchymal and glomerular disease and an independent predictor of progressive kidney disease, cardiovascular disease, and peripheral vascular disease
  • Albumin is the only measurable protein in urine on a urine dipstick. If have a positive urine dipstick for protein (albumin) you need to quantify with either a 24- hour urine collection or protein-creatinine / albumin-creatinine ratio on a random urine sample
  • Level of proteinuria is diagnostically helpful to distinguish tubulointerstitial disease vs glomerular disease ( > 3500 mg/g is glomerular disease; > 150mg/g but < 200 mg/g is tubulointerstitial or glomerular disease)
82
Q

Glomerular Disease

albumin-creatinine ratio interpretation

A

USED TO MEASURE PROTEINURIA

  • If positive and have retinopathy then diagnosis is diabetic nephropathy
  • 30-300 mg/g “microalbuminuria”
  • > 300 mg/g = over proteinuria
83
Q

Glomerular Disease

when to suspect glomerular disease/injury

A

hematuria + proteinuria

84
Q

potential etiologies for AKI

A

Pre-renal:low perfusion (60-70%)
* Hypovolemia, hypotension

Post renal: obstruction to flow (5-10%)
* BPH, urolithiasis, outlet obstruction

Intrarenal: intrinsic disease (25-40%)
* Tubules ( Acute Tubular Necrosis)
* Interstitium (Acute interstitial nephritis)
* Glomerulus (Glomerulonephritis)- RBC casts!! (if you see RBC cases on UA = damage to glomerulus)

85
Q

nephrotic vs nephritic syndrome

A

NEPHROTIC
* UA: fatty casts, > 3.5 g/d proteinuria, +/- hematuria
* preserved absorption of ions, water, creatinine, GFR
* sx: generalized + periorbital edema, HTN

NEPHRITIC
* UA: RBC casts, cola/smoky urine, < 3.5 g/d proteinuria, hematuria
* impaired absorption of ions, proteins, water
* INCREASED creatinine, DECREASED GFR
* sx: edema, HTN

86
Q

Glomerular Disease

causes of focal glomerulonephritis

A
  • Children: benign hematuria, henoch-schonlein purpura, mild post-infectious GN, IgA nephropathy, hereitary nephritis
  • Adults: IgA nephropathy, hereditary nephritis, SLE
87
Q

Glomerular Diseases

causes of diffuse glomerulonephritis

A
  • Children: postinfectious GN, membranoproliferative GN
  • Adults: SLE, membranoproliferative GN, rapidly progressive GN, post-infectious GN, vasculitis
88
Q
A

CMT (78 decks)

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