1
Kidney
- Azotemia, BUN: Cr ratio
● Azotemia: A laboratory diagnosis of elevated BUN & Cr
● Uremia: Is azotemia associated with direct clinical manifestations of renal failure, such as:
○ Pericarditis Increased tendency to bleeding (defective platelet function)
○ Increased liability to infections (defective WBC production)
BUN:CR ratio
● Normally, 15:1
● In renal failure, both BUN & Cr will increased because of the decreased GFR
● We use BUN:Cr ratio to differentiate between the 3 types of acute renal failure (pre-, intra-, and post-renal) making use of the fact that both urea
and creatinine are filtered at the glomerulus but only urea gets reabsorbed, and only creatinine gets secreted at the renal tubules
○ “In the kidney, urea is filtered and reabsorbed (PT 80%).”
○ “In the kidney, creatinine is filtered and secreted (DT), but NOT reabsorbed.”
- The different types and causes of acute renal failure
-Diagnosing the type of renal failure by: Blood tests (BUN, Cr & BUN:Cr ratio) and urine tests
(urine osmolarity, specific gravity, and urine sodium and FENa)
● The most common indicator of acute renal failure is:
○ Azotemia (an accumulation of nitrogenous wastes in the blood) A decrease in glomerular filtration rate (GFR)
○ Clues to the “acuteness”: Normal kidney size, hematocrit, and Ca++
Major causes of acute renal failure (ARF): Prerenal, Renal, and Post-renal
Pre-renal Renal Post-renal
Normal tubules & reabsorption is Reabsorption is lost, Secretion is lost l /t Early: normal tubular function
SUPERnormal (filtrate is slow), secretion is GFR dropping Late: disfunction
normal Mechanism: Problem with the nephron (e.g., Mechanism: Urinary tract obstruction causing back
Mechanism: Low blood flow getting into the glomerulus or tubules) pressure into the kidney
kidney (e.g., low perfusion)
Causes: Causes:
Causes: - Nephrotoxic medications (Aminoglycosides, - Benign prostatic hyperplasia Cervical cancer
- Heart failure Hypovolemia Vancomycin) - Stones (bladder) Neurogenic bladder
- Constrictive pericarditis (liver cirrhosis) - Acute tubular necrosis - Contrast agents
- Renal artery stenosis - Cisplatin (chemotherapy) Blood tests:
- Allergic interstitial nephritis
Blood tests: >> Fever, rash, eosinophils in urine stain by Urine tests:
Sp & US ↑/ C poor NA Hansel’s stain), penicillin, sulfa, phenytoin, Early postrenal ~ 16-19
allopurinol, quinolones, rifampin Late postrenal ~ 11-14
Urine tests: > 20
- Rhabdomyolysis (e.g., crush injury or recent
use of statins > hyperkalemia!) 1. ARF w/ intact tubules
• 2 tests for Sodium: Urine sodium, a) Pre-renal: much better than normal
FE Na+ Blood tests: b) Early post-renal: slightly > normal
• 2 tests for Urine in water: Urine Sp & US ↓/ D rich NA 2. ARF w/ damaged tubules
osmolarity & Sp. Gravity a) Intra-renal: much < than normal
• 1 Blood test: BUN/Cr Urine tests: <1
b) late Post-renal: slightly < normal
- CKD: associated manifestations and their pathophysiological causes. Earliest sign of CKD.
● Progressive loss of kidney function associated with (pathophysiological causes):
○ Systemic disease: Diabetes mellitus, Hypertension
○ Kidney disease: Chronic glomerulonephritis, Chronic pyelonephritis, Obstructive uropathies, or vascular disorders
● Clinical manifestations:
○ CKD is defined as GFR < 60 mL/min/1.73m2 for 3 months or more, irrespective of the cause
○ Initially, no symptoms (only laboratory findings!)
■ Earliest sign: Microalbuminuria, early bone disease, BUN & Cr start to increase
○ Uremia
■ Lethargy Pericarditis Encephalitis
■ Bleeding diathesis Recurrent infections
○ Fluid volume overload
○ Hyper: -kalemia, magnesemia, phosphatemia, and metabolic acidosis
○ was
This study source Hypocalcemia Osteodystrophy
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Neurological Disorders
https://www.coursehero.com/file/239882858/Understanding-Renal-Failure-Causes-Diagnosis-Types/
, 2
- Neurologic disorders: congenital, traumatic, vascular, infectious, degenerative
Congenital
● Neural tube defects
○ Anencephaly The soft, bony component of the skull and part of the brain are missing, spontaneous abortion or early neonatal death
○ Spina bifida occulta Failure of fusion posterior vertebral laminae. Sx due to tethering of SC (gait abnormalities, foot deformities, & bladder
sphincter disturbance)
○ Meningocele A sac-like cyst of meninges filled with spinal fluid, protruding through the vertebral defect
○ Meningomyelocele (spina bifida cystica) Hernial protrusion of a meningocele containing a portion of the spinal cord with its nerves
○ Encephalocele Herniation of the brain and meninges through a defect in the skull
● Congenital hydrocephalus Enlargement of the cerebral ventricles due to blockage of where CSF flows/Pushes and compresses the brain
tissue against the skull cavity, If this develops before fusion of the cranial sutures, the skull can expand to accommodate this additional volume
● Cerebral palsy
○ A group of nonprogressive syndromes that affect the brain and cause motor dysfunction beginning in early infancy
○ Causes
■ Prenatal or perinatal cerebral hypoxia, hemorrhage, or infection
○ Types
■ Spastic (70-80%): Hyperactive deep tendon reflexes, clonus, rigidity
■ Dystonic (10-20%): Difficulty in fine motor coordination, stiff, abrupt movements due to basal ganglia injury
■ Ataxic (5-10%): Manifests with gait disturbance and instability
Traumatic
● Closed (blunt)/open trauma
● Coup/Countercoup injury
● Focal brain injury
○ ⅔ of head injury deaths
○ Example: Extradural hematoma; Subdural hematoma Subarachnoid [CSF] {SAH} (AVM)
■ Extradural hematoma
● Majority: Aterial Lucid interval
■ Subdural hematoma
● Majority: Venous Acute: within hours Subacute: 2 days to 2 weeks
● Chronic: Weeks to months (common in elderly and alcoholics)
● Diffuse brain injury
○ Concussions, Diffuse Axonal Injury (DAI), most of the morbidities
● Primary/Secondary/Tertiary brain injury
○ Primary: Direct result of trauma (e.g., contusion, hematoma)
○ Secondary: Indirect consequences (e.g., cerebral edema, increased ICP)
○ Tertiary: Systemic complications that contribute to further brain injury
Cerebrovascular
● Cerebrovascular accident (CVA, strokes)
○ Thrombotic Embolic Hemorrhagic Lacunar
● Intracranial aneurysms and vascular malformations
● Subarachnoid hemorrhage
Infectious
● Meningitis Bacterial: fever, headache, neck rigidity, and skin in Neisseria Meningitis infections Viral fungal
● Encephalitis Viral
● Brain abscess Usually due to the contiguous spread of infection from the middle ear
Degenerative
● Demyelinating disorders: Multiple sclerosis autoimmune inflammatory disorder, destruction of axonal myelin in the brain & SC
● Parkinson disease (EPS)
○ Degeneration of the basal ganglia “pressing the brakes”, w/ loss of dopamine-producing neurons in the substantia nigra & dorsal striatum
○ Depletion of dopamine (an inhibitory neurotransmitter) & relative excess of acetylcholine (excitatory) activity are manifested by the tremors &
rigidity characterizing the disease
- Cerebellar disorders: manifestations
- Upper motor neuron lesions versus lower motor neuron lesions
- Neurotransmitters:
This role in various
study source was downloaded neurological
by 100000898960505 and
from psychological
CourseHero.com on disorders
05-15-2025 17:09:47 GMT -05:00
https://www.coursehero.com/file/239882858/Understanding-Renal-Failure-Causes-Diagnosis-Types/
Kidney
- Azotemia, BUN: Cr ratio
● Azotemia: A laboratory diagnosis of elevated BUN & Cr
● Uremia: Is azotemia associated with direct clinical manifestations of renal failure, such as:
○ Pericarditis Increased tendency to bleeding (defective platelet function)
○ Increased liability to infections (defective WBC production)
BUN:CR ratio
● Normally, 15:1
● In renal failure, both BUN & Cr will increased because of the decreased GFR
● We use BUN:Cr ratio to differentiate between the 3 types of acute renal failure (pre-, intra-, and post-renal) making use of the fact that both urea
and creatinine are filtered at the glomerulus but only urea gets reabsorbed, and only creatinine gets secreted at the renal tubules
○ “In the kidney, urea is filtered and reabsorbed (PT 80%).”
○ “In the kidney, creatinine is filtered and secreted (DT), but NOT reabsorbed.”
- The different types and causes of acute renal failure
-Diagnosing the type of renal failure by: Blood tests (BUN, Cr & BUN:Cr ratio) and urine tests
(urine osmolarity, specific gravity, and urine sodium and FENa)
● The most common indicator of acute renal failure is:
○ Azotemia (an accumulation of nitrogenous wastes in the blood) A decrease in glomerular filtration rate (GFR)
○ Clues to the “acuteness”: Normal kidney size, hematocrit, and Ca++
Major causes of acute renal failure (ARF): Prerenal, Renal, and Post-renal
Pre-renal Renal Post-renal
Normal tubules & reabsorption is Reabsorption is lost, Secretion is lost l /t Early: normal tubular function
SUPERnormal (filtrate is slow), secretion is GFR dropping Late: disfunction
normal Mechanism: Problem with the nephron (e.g., Mechanism: Urinary tract obstruction causing back
Mechanism: Low blood flow getting into the glomerulus or tubules) pressure into the kidney
kidney (e.g., low perfusion)
Causes: Causes:
Causes: - Nephrotoxic medications (Aminoglycosides, - Benign prostatic hyperplasia Cervical cancer
- Heart failure Hypovolemia Vancomycin) - Stones (bladder) Neurogenic bladder
- Constrictive pericarditis (liver cirrhosis) - Acute tubular necrosis - Contrast agents
- Renal artery stenosis - Cisplatin (chemotherapy) Blood tests:
- Allergic interstitial nephritis
Blood tests: >> Fever, rash, eosinophils in urine stain by Urine tests:
Sp & US ↑/ C poor NA Hansel’s stain), penicillin, sulfa, phenytoin, Early postrenal ~ 16-19
allopurinol, quinolones, rifampin Late postrenal ~ 11-14
Urine tests: > 20
- Rhabdomyolysis (e.g., crush injury or recent
use of statins > hyperkalemia!) 1. ARF w/ intact tubules
• 2 tests for Sodium: Urine sodium, a) Pre-renal: much better than normal
FE Na+ Blood tests: b) Early post-renal: slightly > normal
• 2 tests for Urine in water: Urine Sp & US ↓/ D rich NA 2. ARF w/ damaged tubules
osmolarity & Sp. Gravity a) Intra-renal: much < than normal
• 1 Blood test: BUN/Cr Urine tests: <1
b) late Post-renal: slightly < normal
- CKD: associated manifestations and their pathophysiological causes. Earliest sign of CKD.
● Progressive loss of kidney function associated with (pathophysiological causes):
○ Systemic disease: Diabetes mellitus, Hypertension
○ Kidney disease: Chronic glomerulonephritis, Chronic pyelonephritis, Obstructive uropathies, or vascular disorders
● Clinical manifestations:
○ CKD is defined as GFR < 60 mL/min/1.73m2 for 3 months or more, irrespective of the cause
○ Initially, no symptoms (only laboratory findings!)
■ Earliest sign: Microalbuminuria, early bone disease, BUN & Cr start to increase
○ Uremia
■ Lethargy Pericarditis Encephalitis
■ Bleeding diathesis Recurrent infections
○ Fluid volume overload
○ Hyper: -kalemia, magnesemia, phosphatemia, and metabolic acidosis
○ was
This study source Hypocalcemia Osteodystrophy
downloaded by 100000898960505 Anemia:
from CourseHero.com Lack of EPO
on 05-15-2025 17:09:47 GMT -05:00
Neurological Disorders
https://www.coursehero.com/file/239882858/Understanding-Renal-Failure-Causes-Diagnosis-Types/
, 2
- Neurologic disorders: congenital, traumatic, vascular, infectious, degenerative
Congenital
● Neural tube defects
○ Anencephaly The soft, bony component of the skull and part of the brain are missing, spontaneous abortion or early neonatal death
○ Spina bifida occulta Failure of fusion posterior vertebral laminae. Sx due to tethering of SC (gait abnormalities, foot deformities, & bladder
sphincter disturbance)
○ Meningocele A sac-like cyst of meninges filled with spinal fluid, protruding through the vertebral defect
○ Meningomyelocele (spina bifida cystica) Hernial protrusion of a meningocele containing a portion of the spinal cord with its nerves
○ Encephalocele Herniation of the brain and meninges through a defect in the skull
● Congenital hydrocephalus Enlargement of the cerebral ventricles due to blockage of where CSF flows/Pushes and compresses the brain
tissue against the skull cavity, If this develops before fusion of the cranial sutures, the skull can expand to accommodate this additional volume
● Cerebral palsy
○ A group of nonprogressive syndromes that affect the brain and cause motor dysfunction beginning in early infancy
○ Causes
■ Prenatal or perinatal cerebral hypoxia, hemorrhage, or infection
○ Types
■ Spastic (70-80%): Hyperactive deep tendon reflexes, clonus, rigidity
■ Dystonic (10-20%): Difficulty in fine motor coordination, stiff, abrupt movements due to basal ganglia injury
■ Ataxic (5-10%): Manifests with gait disturbance and instability
Traumatic
● Closed (blunt)/open trauma
● Coup/Countercoup injury
● Focal brain injury
○ ⅔ of head injury deaths
○ Example: Extradural hematoma; Subdural hematoma Subarachnoid [CSF] {SAH} (AVM)
■ Extradural hematoma
● Majority: Aterial Lucid interval
■ Subdural hematoma
● Majority: Venous Acute: within hours Subacute: 2 days to 2 weeks
● Chronic: Weeks to months (common in elderly and alcoholics)
● Diffuse brain injury
○ Concussions, Diffuse Axonal Injury (DAI), most of the morbidities
● Primary/Secondary/Tertiary brain injury
○ Primary: Direct result of trauma (e.g., contusion, hematoma)
○ Secondary: Indirect consequences (e.g., cerebral edema, increased ICP)
○ Tertiary: Systemic complications that contribute to further brain injury
Cerebrovascular
● Cerebrovascular accident (CVA, strokes)
○ Thrombotic Embolic Hemorrhagic Lacunar
● Intracranial aneurysms and vascular malformations
● Subarachnoid hemorrhage
Infectious
● Meningitis Bacterial: fever, headache, neck rigidity, and skin in Neisseria Meningitis infections Viral fungal
● Encephalitis Viral
● Brain abscess Usually due to the contiguous spread of infection from the middle ear
Degenerative
● Demyelinating disorders: Multiple sclerosis autoimmune inflammatory disorder, destruction of axonal myelin in the brain & SC
● Parkinson disease (EPS)
○ Degeneration of the basal ganglia “pressing the brakes”, w/ loss of dopamine-producing neurons in the substantia nigra & dorsal striatum
○ Depletion of dopamine (an inhibitory neurotransmitter) & relative excess of acetylcholine (excitatory) activity are manifested by the tremors &
rigidity characterizing the disease
- Cerebellar disorders: manifestations
- Upper motor neuron lesions versus lower motor neuron lesions
- Neurotransmitters:
This role in various
study source was downloaded neurological
by 100000898960505 and
from psychological
CourseHero.com on disorders
05-15-2025 17:09:47 GMT -05:00
https://www.coursehero.com/file/239882858/Understanding-Renal-Failure-Causes-Diagnosis-Types/
