EXAM 3 REVIEW Flashcards
C5
ELBOW FLEXORS
C6
WRIST EXTENSORS
C7
ELBOW EXTENSORS
C8
FINGER FLEXORS
T1
FINGER ABDUCTORS (LITTLE FINGER)
L2
HIP FLEXORS
L3
KNEE EXTENSORS
L4
ANKLE DORSIFLEXORS
L5
LONG TOE EXTENSORS
S1
ANKLE PLANTAR FLEXORS
How long does spinal shock last (hemodynamic disturbances)
1-3 weeks
Reduction in BP after acute spinal cord injury due to
Loss of sympathetic tone and decreased SVR
Bradycardia from loss of T1-T4 innervation of the heart
Complications 2 years after INJURY in order of from most incidence to least incidence (USCD A-SHPRP)
UTI (59%) Skeletal muscle spasticity (38%) Chills and fever (19%) Decubitus ulcer (16%) Autonomic hyperreflexia (8%) Skeletal muscle contractures (6%) Heterotopic ossicification(3%) PNA (3%) Renal dysfunction (2%) Postop wound infection (2%)
Complications 30 years after INJURY in order of from most incidence to least incidence (DSGC UI-VUMR)
Decubitus ulcer (17%) Skeletal muscle or joint pain (16%) GI dysfunction (14%) CV dysfunction (14%) UTI (14%) ID or Cancer (11%) Visual or hearing disorders (10%) Urinary retention (8%) Male GU dysfunction (7%) Renal Calculi (6%)
Several weeks after acute spinal cord injury, spinal cord reflexes
gradually return, and patients enter a chronic stage
After several weeks after Acute SCI patient enters a chronic stage characterized by
characterized by overactivity of the sympathetic nervous system and involuntary skeletal muscle spasms
Injury at or above C5 =
apnea due to denervation of the diaphragm
Succinylcholine is likely to provoke hyperkalemia
within the
first 6 months after injury (Avoid it after 24 hours of injury)
When does Autonomic hyperreflexia appear?
Appears AFTER spinal shock in association with
return of spinal cord reflexes
Autonomic Hyperreflexia Can be initiated by
cutaneous or visceral stimulation below the level of spinal injury
Autonomic hyperreflexia common stimuli
Surgery or distention of hollow viscus (bladder, rectum) are common stimuli
Autonomic hyperreflexia Stimulation does what? then end result is ?
initiates afferent impulses that enter the spine, this elicits an increase in sympathetic nervous system activity along the splanchnic outflow tract (in normal patients, this is inhibited by higher centers of the CNS) . End result is a Generalized systemic vasoconstriction occurs BELOW the level of the spinal cord injury
Generalized systemic vasoconstriction occur
BELOW the level of the spinal cord injury
Autonomic hyperreflexia patho
- Stimulus below level of spinal cord transection
- Activation of preganglionic sympathetic nerves
- Vasoconstriction
- Hypertension
- Carotid sinus
- Vasodilation /Bradycardia
- Activation of pre-ganglionic sympathetic nerves
What is the hallmark of autonomic hyperreflexia?
Hypertension and REFLEX BRADYCARIDIA (carotid sinus stimulation)
When there is reflex cutaneous vasodilation ?
Reflex cutaneous vasodilation ABOVE the level of spinal injury (nasal stuffiness)
Autonomic Hyperreflexia Neuro symptoms
Headache, blurred vision = severe hypertension (can lead to LV failure)
Who experienced and DO not experience autonomic hyperreflexia?
85% of patients with lesions above T6 exhibit this reflex, unlikely to be associated below T10
Splanchnic nerve and innervations: GREATER SPLANCHNIC NERVE
T5-T9
Splanchnic nerve and innervations: LESSER SPLANCHNIC NERVE
T10-T11
Splanchnic nerve and innervations: LEAST SPLANCHNIC NERVE
T12
Loss of input from higher centers to these nerves
increase risk of exaggerated autonomic reflexes
T5-T12
***Management for exaggerated autonomic reflexes
prevent it! Have vasodilators available (SNP, hydralazine), can occur in PACU when drugs begin to wear off
Loss of input from higher centers to nerve T5-T9, T10-T11 and T12 leads to
Increase risk of exaggerated autonomic reflexes
what happens to the parts of the body ABOVE the level of the spinal cord lesion
VASODILATATION
When GA is selected, avoid
Succinylcholine 24 hours after injury due to risk of hyperkalemia. use NDNMB agents
Autonomic Hyperreflexia occurs in patients with spinal cord injury what level
Above T6
CREST Syndrome
Calcinosis: Calcium deposits in the skin
Raynaud’s Phenomenon: Spasm of blood vessels with
cold or stress.
Esophageal dysfunction: Acid reflux and decrease
esophageal motility.
Sclerodactyly: Thickening and tightening of the skin on
fingers and hands.
Telangiectasias: Dilation of capillaries causing red
marks on skin surface
3 main problems with MARFAN (HPK)
High Arched palare
Pectus excavatum (spoon chest)
Kyphoscoliosis
Marfan’s syndrome most deaths caused by
Cardiovascular
Most common cause of
Mitral Prolapse
Mitral Regurgitation
Mitral stenosis
Snap
MVP
Mid systolic click late systolic murmur
Aortic issue with Marfan
Aortic dilation
Aortic dissection or rupture
Issue with Marfan and CT
Defective CT in aorta and heart valves.
Cardiac Conduction abnormality with Marfan is
BBB common
Respiratory with Marfan 2 common developments
Early development of emphysema
High incidence of spontaneous pneumothorax
Marfan’s Syndrome Anesthesia Considerations
Mainly focus on ?
CV Focus on cardiopulmonary abnormalities
Marfan’s syndrome patients and AIRWAY
Susceptible to temporomandibular joint dislocation
→caution with jaw thrusting
Marfan syndrome and BP considerations
AVOID any sustained increase in systemic blood pressure r/t increased risk of aortic dissection
Marfan and monitoring
Invasive monitoring including TEE consideration in selected patients
High risk for the development of pneumothorax
What kind of patients –>
Marfan’s syndrome
FORMAL DIAGNOSIS of ARF
• INCREASED SERUM CREATININE MORE THAN 0.5 MG/DL OF BASELINE
• 50% DECREASE IN CREATININE CLEARANCE
• A CHANGE IN SERUM CREATININE OF GREATER THAN 0.3 MG/DL WITHIN 48 HOURS OF
ACUTE INSULT
RENAL BLOOD FLOW (RBF) (AUTOREGULATED @
50 TO 150 MMHG
Most susceptible cause ➔
RENAL TUBULE ISCHEMIA (MOST SUSCEPTIBLE) ➔ PROLONGED ➔ IRREVERSIBLE CORTICAL NECROSIS.
Chronic Renal Failure
HYPERKALEMIA, HYPERMAGNESEMIA, HYPERPHOSPHATEMIA, HYPOCALCEMIA
CRF METABOLIC ACIDOSIS -ANEMIA
INCREASED CO, RIGHT SHIFT OF OXYHEMOGLOBIN DISSOCIATION CURVE
Lumbar lordosis/kyphoscoliosis and neuraxial
⇧neuraxial technical difficulty and positioning concerns
EHLERS – DANLOS SYNDROME and neuraxial
Bleeding: Avoid IM injections; excessive instrumentation of nose or esophagus; laryngoscopy; A line or CVP (hematoma);
no regional anesthesia (too much bleeding)
Achondroplasia Dwarfism, Small epidural space =
difficult to introduce epidural catheter
Osteophytes, prolapsed intervertebral discs, or deformed vertebral bodies also contribute to difficulties with neuraxial blockade
Duschenne Muscular Dystrophy and Regional anesthesia
avoids the unique risks of general anesthesia in Duschenne Muscular Dystrophy.
Nemaline Rod Muscular dystrophy Regional anesthesia
high motor block could = respiratory compromise
Myotonic dystrophy:
GA, regional and NMB do NOT prevent/relieve contraction
High concentrations of VA may
decrease contractions but will also cause myocardial depression
What is Nemaline Rod Muscular Dystrophy is a
Slowly progressive symmetrical dystrophy of skeletal and smooth muscles.
Nemaline Rod Muscular Dystrophy and motor
Delayed motor development; muscle weakness; hypotonia, abnormal gait, and loss of deep tendon reflexes
Nemaline Rod Muscular Dystrophy Facial
Micrognathia, dental malocclusion
Nemaline Rod Muscular Dystrophy Skeletal abnormalities
Kyphoscoliosis and pectus excavatum
Heart and Nemaline Rod Muscular Dystrophy
Dilated cardiomyopathy ➔ cardiac failure.
Nemaline Rod Muscular Dystrophy NEURO
Normal mentation
Nemaline Rod Muscular Dystrophy Anesthesia Consideration : INTUBATION
- Difficult tracheal intubation due to micrognathia and high arched palate
- Awake fiberoptic endotracheal intubation may be needed
Nemaline Rod Anesthesia Consideration Respiratory
Respiratory depressant effects of drugs may be exaggerated d/t respiratory muscle weakness and chest wall abnormalities
Nemaline Rod Anesthesia Considerations: Ventilation
V/Q mismatch increased; ventilatory response to CO2 may be blunted
Nemaline Rod Anesthesia Considerations: MUSCLE RELAXANTS
Sux and NDNMB response is unpredictable
Not been reported with Nemaline Rod
MH
What is Periodic Paralysis?
Intermittent acute attacks to skeletal muscle ➔ weakness or paralysis
Causes of Periodic Paralysis
hypo or hyperkalemia
Anesthesia Considerations for PERIODIC PARALYSIS 2 meds
- Acetazolamide
2. Mannitol
Monitor this and AVOID 2 meds in Periodic Paralysis
Frequent K+ monitoring
Avoid potassium solutions
Avoid succinylcholine
Treatment for Periodic Paralysis
Administer glucose containing solutions if treating hyperK c/insulin
Clinical Features of Familial Periodic Paralysis Type: HYPOKALEMIA K value
<3.0
Clinical Features of Familial Periodic Paralysis Type: HYPOKALEMIA : PRECIPITATING FACTORS
PAMGHHSS- CE
Pregnancy Anesthesia Menstruation Glucose infusion HIgh Carb meal Hypothermia Strenuous Exercise Stress
Cardiac Dysrhythmias
ECG signs of Hypokalemia
Clinical Features of Familial Periodic Paralysis Type: HYPERKALEMIA K value
> 5.5
Clinical Features of Familial Periodic Paralysis Type: HYPERKALEMIA : PRECIPITATING FACTORS
PHEM
Potassium Infusion
Hypothermia
Exercise
Metabolic Acidosis
Clinical Features of Familial Periodic Paralysis Type: HYPERKALEMIA: OTHER FEATURES
Skeletal muscle weakness may be localized to tongue and eyelids
MYASTHENIA GRAVIS - What is MG
Chronic autoimmune disorder caused by a decrease in functional acetylcholine receptors (AchR) at the NMJ resulting from destruction or inactivation by circulating antibodies
ACH receptor and MG
Down regulation of AchR
2/3 of patient with MG have
Thymic hyperplasia is present in two thirds of patients with myasthenia gravis, and 10% to 15% of these patients have thymomas
What is the Hallmark of MG:
weakness and rapid exhaustion of voluntary muscles with repetitive use
Partial recovery with rest; muscle strength is normal when well rested
MG Initial symptoms:
ptosis, diplopia, and dysphagia
MG and Aspiration
High aspiration risk (Weak pharyngeal, laryngeal muscles = dysphagia, dysarthria and difficulty handling saliva
MG and heart
Myocarditis can result in atrial fib, heart block, or cardiomyopathy
Other autoimmune diseases that may precipitate MG
HPRS
Hyperthyroidism
Pernicious anemia
Rheumatoid arthritis
Systemic lupus erythematosus
What are meds that can aggravate muscle weakness
Antibiotics, especially aminoglycosides, can aggravate muscle weakness
May precipitate or exacerbate muscle weakness in Myasthenia Gravis (PIESE)
Pregnancy Infection Electrolyte abnormalities, Surgery Emotional stress
Treatment of Myasthenia Gravis PIP-T
Pyridostigmine
Immunosuppressive Therapy
Plasmapheresis
Thymectomy
Anesthesia Considerations of Myasthenia GRAVIS
MUSCLE RELAXANTS
⇧ sensitivity to NDNMB; decrease dose by ½ to 2/3 Or just avoid it completely
Resistance to succinylcholine Need 2.6 X the ED95
MG and Volatile agents
VA have MS relaxation properties
Postpone extubation and ventilator support postop.
MYASTHENIC SYNDROME AKA Eaton-Lambert Syndrome
What is it?
Resembles Myasthenia Gravis IgG antibodies attack Ca2+ channels
Treatment of Myasthenic Syndrome
3,4 Diaminopyridine
• IgG (6 to 8 weeks).
Myasthenia syndrome Anesthesia Considerations
Sensitive to depolarizing and non-depolarizing NMB
Antagonism of NM-Blockade with anticholinesterase drugs may be inadequate.
The potential presence of myasthenic syndrome and the need to decrease doses of muscle relaxants should be
Considered when?
considered in patients undergoing bronchoscopy, mediastinoscopy, or thoracoscopy***for suspected lung cancer
Epidermolysis Bullosa Despite
dystrophic skeletal muscle, no increased risk of a hyperkalemic response when treated with succinylcholine
Scleroderma Musculoskeletal system:
myopathy- weak, mostly proximal skeletal muscle groups
EHLER”S DANLOS SYNDROME Musculoskeletal: Joint
hypermobility, musculoskeletal discomfort, susceptibility to osteoarthritis.
DERMATOMYOSIS
Abnormal immune responses ➔ Slow, progressive skeletal muscle damage
S/ S of Dermatomyosis S
keletal muscle weakness (e.g., difficulty climbing stairs) d/t skeletal muscle destruction ➔ increased serum creatine kinase levels.Neuromuscular junction is not affected
Neuromuscular junction is not affected
Dermatomyosis
Marfan’s Syndrome Additional skeletal abnormalities
PKHH
Pectus excavatum
Kyphoscoliosis
Hyperextensibility of the joints
High-arched palate
Duschenne Muscular dystrophy Group of
hereditary diseases characterized by painless degeneration and atrophy of skeletal muscles
Duschenne Muscular Dystrophy
Progressive, symmetrical skeletal muscle weakness and wasting but no evidence of skeletal muscle denervation
Initial symptoms of Duschenne Muscular Dystrophy
waddling gait, frequent falling, difficulty climbing stairs, and these reflect involvement of the proximal skeletal muscle groups of the pelvic girdle
Affected muscles become larger as a result of fatty infiltration
Duschenne Muscular dystrophy and ambulation
Predispose to ?
Typically confined to a wheelchair by age 8 to 10
Skeletal muscle atrophy can predispose to long bone fractures
PRADER WILLI SYNDROME and skeletal
Weak skeletal musculature = poor cough and ⇧pneumonia
Systemic Lupus Erythematous *(SLE) is a
Multisystem chronic inflammatory disease characterized by antinuclear antibody production
SLE exacerbated by
Exacerbated by infection, pregnancy, surgery
SLE Onset can be drug induced: PHIDA
Procainamide hydralazine Isoniazide, D - penicillamine ALpha - methyldopa
Treatment of SLE (CIB)
Corticosteroids
Immunosuppressive treatment
Bone marrow transplant
Anesthesia Considerations for SLE
CRML
Laryngeal involvement
Mucosal ulceration
Cricoarytenoid arthritis
Recurrent laryngeal nerve palsy, may be present in as many as 1/3 patients
Periodic Paralysis: Avoid
Potassium solutions
Periodic Paralysis: CAUSES
HYPO and HYPERKALEMIA
Epidermolysis Bullosa and K+ and SUCC
NO INCREASED OF HYPERKALEMIC RESPONSE WITH SUX
Duschenne Muscular dystrophy Succinylcholine
contraindicated d/t risk of rhabdomyolysis, hyperkalemia, and/or cardiac arrest -
Duschenne Muscular dystrophy: VA
Rhabdomyolysis, with or without cardiac arrest, observed with administration of VOLATILE anesthetics to these patients even in the absence of succinylcholine
What is Mastocytosis
Rare; disorder of mast cell proliferation; degranulation of mast cells
Mastocytosis Urticaria pigmentosa is usually
benign and asymptomatic
Children are most often affected → resolves by adulthood
Systemic mastocytosis : What happens
mast cells proliferate in all organs (especially bone, liver, and spleen, but not in the CNS).
Signs and Symptoms of Mastocytosis
Histamine release from mast cells and prostaglandins are involved➔ anaphylactoid responses characterized by pruritus, urticaria, and flushing with hypotension (life threatening) and tachycardia
Mastocytosis and bronchospasm,
Low risk of bronchospasm Bleeding unusual, even though mast cells contain heparin!
Anesthetics Management for MASTOCYTOSIS Influenced by
the possibility of intraoperative mast cell degranulation and anaphylactoid reaction
-Have epinephrine readily available
Mastocytosis : Contrast dye
has caused profound hypotension- pretreat with H1,H2 blockers and glucocorticoid
Mastocytosis and Cromolyn-
inhibits mast cell degranulation, i.e. release of histamine (also used to treat asthma) -
Mastocytosis Safe: VVPF
Volatile anesthetics,
Vecuronium.
Propofol
Fentanyl
Mastocytosis Avoid:
Succinylcholine and Meperidine may cause mast cell degranulation
Upper cervical spine most at risk
(C1-C3)
Morbidity and mortality for cervical injuries include
alveolar hypoventilation with inability to clear bronchial secretions, plus the risk of aspiration of gastric contents, pneumonia, and pulmonary embolism (slide 5)
Lateral protrusion of a cervical disk usually occurs at
C5-6 or C6-7 intervertebral spaces
Symptoms can be exaggerated by coughing
CERVICAL INJURY Management of anesthesia: primary concern is
airway approach, direct laryngoscopy should only be done if no significant worsening of symptoms occur with neck movement (especially extension)
Management of anesthesia: cervical spine procedures via the anterior approach
involves retraction of the airway structures and may result in injury to the ipsilateral recurrent laryngeal nerve and can manifest as hoarseness, stridor, or frank airway compromise
MANAGEMENT OF CERVICAL SPINE PROCEDURES Compression of
Recurrent laryngeal nerve fibers can be caused by the endotracheal tube or the inflated cuff. It is common practice to decrease the cuff completely and reinflate it until a leak is no longer heard
Cervical spondylosis =
neck pain and radicular pain in the arms and shoulders accompanied by sensory loss and skeletal muscle wasting. Later, sensory and motor signs may appear in the legs producing an unsteady gait
UNSTABLE C-NECK
Sensitivity of plain radiographs for detecting cervical spine _____THEREFORE
injury is < 100%, treat all acute cervical spine injuries as potentially unstable
Immediate immobilization to limit
neck flexion/extension
Manual in-line stabilization during laryngoscopy
CERVICAL SPINE movement tend to
Movement tends to occur in the occipito-atlanto-axial area even with stabilization
Neck hyperextension can further
damage the spinal cord
Anesthetic implications for old spinal injury. Chronic spinal cord injuries lead to ICACAA
Impaired alveolar ventilation Cardiovascular instability Autonomic hyperreflexia), Chronic pulmonary and genitourinary tract infections, Anemia Altered thermoregulation
Chronic spinal cord injuries and renal
Renal failure can occur
Anesthetic implications for old spinal injury.Immobility leads to
osteoporosis, skeletal muscle atrophy, DVT/VTE, pathologic fractures
Several weeks after acute spinal cord injury,
spinal cord reflexes gradually return, and patients enter a chronic stage characterized by overactivity of the sympathetic nervous system and involuntary skeletal muscle spasms
Spasm with spinal cord injury Medication to help and how it works
Baclofen
potentiates GABA) is useful to treat spasticity (abrupt withdrawal = seizures
Chronic Spinal Cord Injury
Injury at or above C5 there is ______Due to
apnea due to denervation of the diaphragm
Even when the diaphragm is intact, coughing and the ability to clear secretions from airway may be impaired due to denervation of intercostal and abdominal muscles
Injury at or above C5 RESPIRATORY CHANGES
What does anesthetist need to do? What can occur?
Marked decreased vital capacity, arterial hypoxemia Need to preoxygenate before suctioning (bradycardia or cardiac arrest can occur)
Chronic Spinal Cord Injury Management of Anesthesia
Prevent autonomic hyperreflexia
Chronic Spinal Cord Injury Management of Anesthesia; Muscle Relaxant
Use NDNMB to prevent reflex skeletal muscle spasms in response to surgical stimulation
Chronic Spinal Cord Injury Management of Anesthesia: SUCC
Succinylcholine is likely to provoke hyperkalemia within the first 6 months after injury (Avoid it after 24 hours of injury)
Chronic Spinal Cord Injury Management of Anesthesia: ANTICIPATE what? What medication not to stop ?
Anticipate altered hemodynamics
Continue Baclofen and benzodiazepines perioperatively
What is Amyotrophic Lateral Sclerosis (ALS)
Degenerative disease involving the lower motor neurons in the anterior horn gray matter of the spinal cord and the corticospinal tracts (primary descending upper motor neurons)
ALS produces
Produces both upper and lower motor neuron degeneration
Most common affected with ALS
Most commonly affects men 40-60 years of age
ALS: Primary lateral sclerosis
= limited to the motor cortex of the brain
ALS Pseudobulbar palsy =
limitation to the brainstem nuclei
Amyotrophic Lateral Sclerosis Symptoms reflect and resemble what?
upper and lower motor neuron dysfunction (resembles myasthenia gravis)
ALS Begins with
Skeletal muscle atrophy
Weakness
Fasciculations in the hands
Eventually includes all skeletal muscles including the tongue, pharynx, larynx, and chest TPLC
ALS Bulbar involvement includes
fasciculations of the tongue plus dysphagia, which leads to pulmonary aspiration
With ALS Autonomic nervous system dysfunction can be manifested as
Orthostatic hypotension and resting tachycardia
Muscles Spared with ALS
Ocular muscles are spared
Amyotrophic Lateral Sclerosis Anesthesia considerations: RESPIRATORY
Exaggerated respiratory depression
Amyotrophic Lateral Sclerosis Anesthesia considerations
Vulnerable to
Vulnerable to hyperkalemia following succinylcholine administration
Amyotrophic Lateral Sclerosis Anesthesia considerations NDNMB
Prolonged responses to NDNMBA
What predisposes ALS patients to aspiration
Bulbar involvement predisposes to pulmonary aspiration
Syringomyelia (syrinx) is a disorder where there is
cystic cavitation of the spinal cord
Syringomyelia (syrinx) What is called syringobulbia?
Rostral extension into the brainstem
Syringomyelia (syrinx) - Communicating syringomyelia =
Either only dilation of the central canal of the cord (hydromyelia) or there is communication between the abnormal cystic lesions in the spinal cord proper and the CSF spaces
Syringomyelia - What is communicating syringomyelia associated with?
Associated with basilar arachnoiditis or Chiari’s malformation
Syringomyelia- Noncommunicating syringomyelia =
presence of cysts that have no connection to the CSF spaces
Syringomyelia Symptoms:
sensory impairment involving pain and temperature sensation in the upper extremities (destruction of neuronal pathways), as cavitation progresses, destruction of lower motor neurons ensues causing skeletal muscle weakness and wasting and loss of reflexes
Syringomyelia Thoracic scoliosis why?
Thoracic scoliosis can result from weakness of paravertebral muscles
Syringobulbia
paralysis of the palate, tongue, and vocal cords
Syringomyelia Management of anesthesia:
TEAT
Thoracic scoliosis can cause V/Q mismatching
Avoid succinylcholine due to lower motor neuron disease
Exaggerated responses to nondepolarizing muscle relaxants
Thermal regulation may be impaired
GFR
best measure of renal function • normal: > 90 ml/min
Creatinine clearance •
Most reliable measure of GFR
Normal CrCL
110-140ml/min
Serum creatinine
Normal: 0.6 to 1.3 mg/dl
Blood urea nitrogen (bun) • normal:
10 to 20 mg/dl
Function of Renal system
Sodium and water removal
Waste removal
Hormone production
Kidney Filter the plasma volume every
22 minutes
3 things kidney regulate OVP
- Regulation of plasma osmolarity
- Regulaiton of plasma volume
- Regulation of arterial pH (acid-base)
3 things kidney regulate OVP
Regulation of plasma osmolarity
Regulaiton of plasma volume
Regulation of arterial pH (acid-base)
Kidney Removal of
metabolic water and foreign substances (urea and drugs)
Kidney produces and activation of
Production of erythropoietin and renin
Actionvation of Vitamin D 3
Fluid overload problems in kidneys
Elevated wastes products (Urea, creatinine, potassium)
Changes in hormone control in the kidney (BUM)
Blood pressure
Making RBCs
Uptake of calcium
Filtration is
movement of fluid from glomerulus to Bowman’s capsule
Tubular Reabsorption is
Movement from Bowman’s capsule to Peritubular capillaries
Tubular Secretion is
Movement from Peritubular capillaries to Bowman’s capsule
Proximal tubule NaGluKAHPPUH
reabsorption of NaCL Glucose K Amino Acids HCO3 PO4 Protein Ureak H2O ( ADH not required)
Tonicity of fluid (within ducts) Proximal
Isotonic
Tonicity of fluid (within ducts) Loop of Henle
Isotonic, Hypertonic, Hypotonic
Tonicity of fluid (within ducts) Distal
Isotonic or Hypotonic
Tonicity of fluid (within ducts) Collecting duct
Final Concentration
Proximal tubule Secretion of (HFOI)
H+
Foreign Substances
Organic Anions, Catiion
Isotonic
Where is ADH not required
Proximal
LOOP of HENLE (CADU)
Concentration of urine (countercurrent mechanism)
Ascending loop Na+ Reabsorbed (active transport, water stays in)
Descending loop WATER Reabsorbed Nacl diffuses in
Urea secretion in thin segment
Distal Tubule NHH
KUHNS
Reabsorption of NaCL, H2O (ADH required) HCO3 Secretion of KUHNS K+ Urea H+ NH3+ Some drugs
Distal Tubule NHH KUHNSI
Reabsorption of NaCL, H2O (ADH required) HCO3 Secretion of KUHNSI K+ Urea H+ NH3+ Some drugs Iso or Hypo
Connecting Tubule Reabsorption of
H2O (ADH required)
COLLECTING Reabsoprtion OR secretion of NaKHN
Na+
K+
H+
NH3+