FLUIDS AND ELECTROLYTES (8-10 QS, SOME INTEGRATED WITH RENAL)

Know the Magic Numbers for…

• Sodium: 135-145
• Potassium: 3.5-5
• Calcium: 8.5-10.5
Role of ADH and Aldosterone..
• What does ADH do in the loop and where in the loop?
o
• What does Aldosterone do and where in the loop?
o
• Remember that ADH works on fluid only
• Aldosterone works on sodium and by retaining sodium it’s going to cause what to happen
to potassium?
o When sodium is retained the kidneys excrete more potassium which can cause
low potassium levels in the body.
• What happens to water when sodium is held back in?
o When sodium is retained it pulls water into the bloodstream and tissues.
• Remember where sodium goes there goes water.
• BUN is indicative when there is a renal problem but it is not the most substantial or most
important lab value because dehydration and overhydration cant affect it. The same thing
with the hematocrit.

How do they control fluid and which electrolytes are influenced?

• ADH:
o ADH increases water reabsorption in the kidneys by making the collecting ducts
more permeable to water.
o Primary regulator of water excretion.
o adjust electrolyte levels by modifying kidney function.
• Aldosterone:
 o Aldosterone promotes reabsorption of sodium and water in the kidneys, primarily
in the distal tubules and collecting ducts.
o Stimulation of the hormone aldosterone increases reabsorption of sodium, and
subsequently, water, in the renal tubules.
o Aldosterone: increases sodium reabsorption and potassium excretion.
o Aldosterone: adjust electrolyte levels by modifying kidney function.
What area of the kidneys do these influence?
• ADH: Regulates fluid. Affects kidneys by making the distal convoluted tubule and
collecting ducts more permeable to water.
• Aldosterone: Regulates sodium. Works on the distal convoluted tubule to retain sodium,
causing potassium to be excreted.
What laboratory tests indicated dehydration and over hydration?
• Dehydration: Elevated BUN and elevated hematocrit
• Overhydration: Low BUN and low hematocrit
• BUN range: 7-20 mg/dL
• Hematocrit range: Female: 36%-48% Male: 39%-54%
Know the signs and symptoms of the following electrolyte disorders:
Hypernatremia

• Fluid Shift: Water shifts from intracellular to extracellular space, causing cellular
dehydration.
• Causes:
o Dehydration: Inadequate water intake, excessive water loss (e.g., fever, burns,
diabetes insipidus).
o Excess Sodium Intake: Hypertonic saline, sodium bicarbonate.
• Symptoms:
o Thirst
o Confusion, irritability
o Muscle twitching
o Seizures, coma

Hyponatremia (where is the fluid shift)

• Fluid Shift: Water moves into cells, leading to cellular swelling (risk of brain edema).

Causes:

• Excess Water Intake: Dilutes sodium (e.g., polydipsia, SIADH).

• Fluid Retention Conditions: Heart failure, kidney disease, liver cirrhosis.

Symptoms:

• Nausea, vomiting, diarrhea

• Headache, lethargy, confusion
• Seizures, coma
• Fluid excess signs such as edema

Hyperkalemia

• Pathophysiology: Increased cell excitability, affecting cardiac and neuromuscular function.

Causes:

• Renal Failure: Inability to excrete potassium.

• Cellular Injury: Trauma, burns causing potassium release. • Medications: Potassium-sparing
diuretics, ACE inhibitors.

Symptoms:

• Neuromuscular: Muscle weakness, paresthesia, cramps.

• Cardiac: Dysrhythmias, risk of cardiac arrest.
• EKG Changes: Peaked T waves, widened QRS, ventricular fibrillation

Hypokalemia

• Pathophysiology: Reduced cell excitability, leading to muscle dysfunction.

Causes:

• Inadequate Intake: Poor diet.

• Excessive Losses: Diuretics, vomiting, diarrhea. • Metabolic Alkalosis.

Symptoms:

• Neuromuscular: Weakness, cramping, paresthesia, hyporeflexia.

• GI: Constipation.
• Cardiac: Arrhythmias, premature ventricular contractions.
• EKG Changes: Flattened T waves, U waves, ventricular tachycardia

What is the role of magnesium in potassium disorders?

• Magnesium plays a critical role in potassium balance.

• Hypomagnesemia (Low Magnesium <1.5 mEq/L) can cause refractory hypokalemia:

• Mechanism: Magnesium regulates potassium transport in cells. When magnesium is low,

potassium cannot be effectively retained by cells, leading to persistent hypokalemia despite
potassium supplementation.

• Clinical Practice: If potassium levels remain low despite supplementation, magnesium levels
must be corrected first

Hypercalcemia (calcium quiets)

• Pathophysiology: Calcium “quiets” neuromuscular activity, leading to decreased excitability.

Causes:
• Hyperparathyroidism (Excess PTH).
• Malignancy (Bone metastasis releases calcium).
• Excessive Intake: High calcium or vitamin D intake.

Symptoms:

• Fatigue, weakness
• Lethargy, personality changes, headache
• Cardiac: Shortened QT interval, atrioventricular blocks
• Kidney stones
• Osteopenia/osteoporosis

Hypocalcemia

• Pathophysiology: Increased neuromuscular excitability, leading to spasms and hyperreflexia.

Causes:

• Hypoparathyroidism (Low PTH).

• Vitamin D Deficiency (Impaired calcium absorption).

• Renal Disease, pancreatitis.

Symptoms:

• Neuromuscular: Tetany, muscle cramps, tremors, seizures.

• Positive Chvostek and Trousseau Signs.
• Cardiac: Prolonged QT interval, risk of ventricular dysrhythmias

RENAL (6 QUESTIONS)

Know what parts of the nephron absorb sodium, potassium, and fluid
• Sodium: Loop of Henle
• Potassium: Proximal Convoluted Tubule
• Fluid: Proximal Convoluted Tubule

How do ADH and Aldosterone affect the nephron and where?

• ADH and Aldosterone change the excretion rate of Na in
the Distal Convoluted Tubule. This mechanism assists in BP regulation along with renal
blood flow.

Know what the GFR indicates

• GFR: the speed at which the blood moves through the glomerulus.
• Can be calculated with a formula that considers age, sex, and ethnicity.
• 90-125 is normal
• below 60 indicates kidney disease
• 15 indicates kidney failure.

Recognize the role of RAAS in controlling BP

• Renin is released from the juxtaglomerular cells. Renin acts on Angiotensinogen to
form Angiotensin I. The liver produces angiotensinogen and releases it into the
bloodstream. Angiotensin I is converted to Angiotensin II by ACE in the
lung. Angiotensin II directly raises BP by constricting blood vessels. Angiotensin
II also stimulates the thirst center in the brain, increases ADH and Aldosterone which
further help in BP regulation.

What substances are part of the RAAS and what do they do?
• Hormone system that regulates the BP and fluid balance.
• Renin (1st hormone in the cascade) – enzyme secreted by the kidneys in response to
low bp, low Na+. or sympathetic nervous system activation.
 - Released in juxtaglomerular cells.
• Angiotensin – protein that, when activated constricts blood vessels and raises BP.
• Aldosterone – a hormone that promotes sodium and water retention;
increasing BP and blood volume.

What is the kidney’s responsibility ion tree blood cell production?

• The kidney secretes erythropoietin (EPO), which stimulates bone marrow to produce
RBCs.

ACID-BASE BALANCE (5-6 QS INTEGRATED IN RENAL AND RESP DISORDERS)

Know magic numbers for…

• pH range: 7.35-7.45

• BUN: 6-20 (8-23 older adult)

• Creatinine: .7-1.3 (men) .6-1.1 (women)
• BicarB: 22-26
• C02: 35-45
 Be able to recognize difference between…

Respiratory acidosis

• pH < 7.35
pCO2 > 45mmHg
• Blood pH DECREASES to 7.35 due to INCREASED CO2 levels. Can be caused by
HYPOVENTILATION due to factors such as:
o COPD, Respiratory Muscle Weakness, Sedative Overdose
• Mechanism - CO2 accumulation increases carbonic acid which dissociates to release
hydrogen ions (H+), lowering pH.
• Symptoms - Headache, confusion, drowsiness, in severe cases coma
• Immediate Response:
o Buffers in blood work to temporarily stabilize pH
• Renal Compensation:
o Kidneys increase bicarbonate reabsorption and hydrogen ion excretion to raise pH
• Duration:
o Renal compensation takes HOURS to DAYS to effectively stabilize blood pH.

Respiratory Alkalosis

• pH > 7.45
pCO2 < 35mmHg
• Blood pH INCREASES above 7.45 due to decreased CO2 levels, often caused by
HYPERVENTILATION such as:
o Anxiety, Panic Attacks, Fever, Sepsis, Pain or High Mechanical Ventilation
• Mechanism -Excessive CO2 loss reduces carbonic acid levels, decreasing hydrogen ions
and raising pH
• Symptoms - Dizziness, numbness, muscle spasms, occasionally LOC
• Immediate Response:
o Blood buffers release hydrogen ions to counteract the rise in pK
 • Renal Compensation:
o Kidneys excrete bicarbonate and retain hydrogen ions to lower pH slowly
• Duration: Can take hours to days to adjust
• Treatment: Treat underlying cause by reducing anxiety, correct hypoxia, breathe into a
paperboy.

Metabolic Acidosis

• pH < 7.35
Bicarb (HCO3) < 22 mEq/L
• Blood pH DECREASES due to excessive acid production or bicarbonate loss, usually
due to conditions that increase acid or reduce bicarbonate such as:
o Diabetic Ketoacidosis, Renal Failure, Severe Diarrhea (loss of bicarbonate)
• Mechanism: Accumulation of non-volatile acids (lactic acid) or bicarbonate deficit
decreases pH
• Symptoms: Rapid breathing (Kussmaul respirations), fatigue, confusion, and in severe
cases shock
• Immediate Response:
o Blood buffers neutralize excess hydrogen ions to limit pH drop
• Respiratory Compensation:
o Lungs increase breathing rate to exhale more CO2, reducing acidity
• Duration: Respiratory mechanism is rapid, providing a quick response to pH
disturbances

Metabolic Alkalosis

• pH > 7.45
Bicarb (HCO3) > 26mEq/L
• Blood pH INCREASES due to excess bicarbonate or loss of acid due to reasons such as:
 o Vomiting or gastric suction, excessive intake of anti-acids, diuretic use leading to
excessive bicarbonate retention
• Mechanism: Increased bicarbonate concentration or acid loss RAISES blood ph
• Symptoms: Irritability, muscle cramps, twitching, and in severe cases cardiac
arrhythmias
• Immediate Response:
o Buffers release hydrogen ions to decrease blood pH slightly
• Respiratory Compensation:
o Lungs reduce breathing rate to retain CO2 increasing blood acidity Duration:
Occur quickly, within minutes to hours

If given a set of values, be able to determine type of acidosis or alkalosis NOTHING on

compensation
• PRACTICE!! What am I? Start with pH, is it acidosis <7.35 OR alkalosis >7.45,
then move to CO2 and HCO3. The one that’s abnormal is your system that’s fucked
up. :)
Be able to explain how the kidneys and lungs compensate for changes in pH

Regulation of pH

Respiratory:

• Regulates blood pH through carbon dioxide exhalation Fast-acting but temporary

adjustments
• CO2 produced by cell metabolism is covered to carbonic acid (H2CO3) in blood, which
releases H+ ions, increasing acidity
By exhaling CO2, the respiratory system reduces the acid load and helps raise pH
• Can rapidly adjust pH by altering breathing rate

Mechanism of Respiratory Regulation

 • Hyperventilation - response to acidosis, expels more CO2 Hypoventilation - response to
alkalosis, breathing slowed to retain CO2

Renal System:

• Controls pH by managing bicarbonate (HCO3) reabsorption and hydrogen ion (H+)

excretion
Slower response, provides long-term pH stability

Role of Regulation

• Reabsorb bicarbonate ions and excrete hydrogen ions.

Produce new bicarbonate ions to help buffer any additional acid in blood Process can take
hours or days, more stable long term solution

pH = 7.50 CO2 = 25 HCO3 = 23 pH = 7.65 CO2 = 40 HCO3 = 35

pH = 7.25 CO2 = 36 HCO = 19 pH = 7.15 CO2 = 80 HCO3 = 24

Recognize which conditions cause specific acid-base balance disorders

Types Causes
Respiratory Acidosis
COPD, Respiratory Muscle Weakness,
Not breathing CO2 out effectively, retaining too Sedative Overdose
much.
Respiratory Alkalosis Anxiety, Panic Attacks, Fever, Sepsis, Pain or
Blowing out CO2 too much with rapid breathing High Mechanical Ventilation
Metabolic Acidosis
Diabetic Ketoacidosis, Rhabdomyolysis,
Losing bases from diarrhea and poor hydrogen Renal Failure, Severe Diarrhea (loss of
ion excretion due to impaired kidney function. bicarbonate)
Lactic acid build up from DKA or rhabdo.
Metabolic Alkalosis
Vomiting or gastric suction, excessive intake
of anti-acids, diuretic use leading to excessive
Acids lost in stomach secretions, too much bases
bicarbonate retention
infected form anti-acid medicine.

CHRONIC BRONCHITIS (4-5 QUESTIONS)

What are the pathophysiology and risk factors involved in chronic bronchitis?
• Pathophysiology: The bronchial walls thicken and hypertrophy of mucus glands occurs.
• Bronchial walls are thickened d/t chronic inflammation
• Chronic inflammation d/t inflammatory mediators (cytokines, mostly) recruiting immune
cells to bronchial walls, resulting in eventual fibrosis/thickening and smooth muscle
hypertrophy.
• Narrows the airway, resulting in prolonged expiration and air trapping(airway
remodeling)
• Due to same processes above, lungs lose elasticity, further impairing airflow (airway
remodeling)
• Goblet cell hyperplasia (increase in number)
o Main mucus-producing (epithelial) cells that line the airways
§ Increased mucus production in response to inflammation,
which blocksairways
• Cilia in airways are damaged and cannot effectively clear mucus
• Increased risk for infections
• Submucosal gland hypertrophy (get larger)
• Once enlarged, also produce excessive mucus
o leads to airway obstruction
• Overall airway remodeling is the result, which causes prolonged expiration, air trapping,
and eventual loss of elasticity
• Air trapping increases CO2 retention (hypercapnia)
• Mucus/inflammation cause hypoxemia (impaired oxygen transfer across alveoli)
• Need-to-know concepts associated w/pathophysiology:
• Diagnostic criteria:
• Chronic, productive cough lasting for at least three months of the year for two
consecutive years
• Cough is more prevalent at night d/t pooling of mucus!
• FEV1/FVC ratio <70% confirms airflow limitation
• COPD (and therefore chronic bronchitis) literally changes the respiratory drive
• Normally driven by excess CO2 levels
• In COPD, driven by low O2 levels
• This is why we can’t have COPD pts on >2-4L of O2: It will literally decrease their
respiratory drive (through oxygen ‘toxicity’) and cause respiratory failure!
• COPD (and therefore chronic bronchitis) can cause pulmonary hypertension
• Which we all know causes right-sided heart failure (cor pulmonale)
• One of those odd instances where you can develop right-sided heart
failure without having left-sided heart failure first
• Acute exacerbations worsen symptoms, and the more you have/the worse they get, the
closer you are to calling ya girl to come admit you to the ‘Bye-Bye-Bye’ crew. More
frequent exacerbations are actually the best predictor of more severe, life-threatening
exacerbations. I’ll ask an MD what the koalifications are for our hospice pts this
weekend, as I see COPD and acute/chronic resp failure a LOT as a terminal dx.
• Meds are based on the severity of the COPD (GOLD guidelines): KNOW THE
CONCEPT, NOT THE DEETS. Worse classification = more meds. Exacerbations are a
biggie in determining stage.
• Risk Factors:
o Smoking: Irritates airways, promoting chronic inflammation and mucus
production
o Environmental exposure: Air pollution, dust, chemical fumes (contribute to
chronic irritation of bronchi)
o Occupational hazards: Prolonged exposure to industrial pollutants (e.g., coal dust,
asbestos, etc.)
 o Recurrent respiratory infections: Frequent infections damage airway lining and
promote chronic inflammation.
o Genetic predisposition: Alpha-1 antitrypsin deficiency increases risk for COPDs
o Age: Usually in adults >40 years old
o Socioeconomic factors: Limited access to healthcare increases risk of untreated
infections and chronic inflammation

What differentiates chronic bronchitis from emphysema?

• Areas affected
o Chronic bronchitis affects the bronchi
o Emphysema affects the alveoli (see specific portion of exam review for details)
• Main symptoms
o Chronic bronchitis is persistent, productive cough
o Emphysema is shortness of breath
• Clinical manifestations differences:
•
• Know the pathophysiology behind both in order to understand how they differ conceptually.
When you understand that, you’ll be able to understand the other differences.

Which inflammatory cells are involved and what do they do?

• Macrophages and neutrophils
 o Per PubMed article: “Macrophages are the most representative immune cells in
the respiratory tract, given their role in airways surveillance, cellular
debris removal, immune surveillance, and inflammation resolution.”
o From textbook: “Neutrophils, macrophages, and lymphocytes release
inflammatory mediators (e.g., CD8+ lymphocytes) and oxidants, which infiltrate
the airway… these inflammatory mediators attract more inflammatory cells from
the circulation, enhance the inflammatory response, and start the process of
structural lung changes.”
• They release cytokines, recruit other cells, phagocytize bacteria, and release
inflammatory mediators, all of which inflame the tissue constantly and eventually cause
fibrosis.
• CD8+ T-cells:
o According to her lecture, they ‘dominate the inflammatory response’
• Remember that these are the cytotoxic killer dudes
• The higher the level in the lungs, the more damage being done
• Chemical mediators (mentioned on same slide)
o IL-8: Attracts neutrophils
o Tumor Necrosis Factor-Alpha (TNF-α): Amplifies inflammation
o Proteases: Cause tissue destruction and airway remodeling

What acid-base balance occurs in chronic bronchitis?

• The COPDs cause air trapping, so air cannot get out… meaning we retain more
CO2. (Remember what I said ^^^ up there about respiratory drive changing to low
O2 rather than excess CO2: COPD pts always retain CO2, so the drive changes to
low O2 instead to keep respiratory drive going.)
• If we retain CO2, it interacts w/water in our bodies to form carbonic acid (H+ ions
are released)
• If we’re becoming acidic and it’s because of a breathing issue, it’s respiratory
acidosis
EMPHYSEMA (4-5 QUESTIONS)

What is the pathophysiology and risk factors for emphysema?

• ● Emphysema is a chronic, progressive lung disease classified under Chronic

Obstructive Pulmonary Disease (COPD).
• ● Primary issue:
o Destruction alveolar walls —> loss of elasticity —> air trapping —->
hyperinflation of the lungs
• ● Reduced surface area for gas exchange —> poor O2 and CO2 exchange
• ● Structural changes:
o Bullae formation: Large air spaces form due to alveolar destruction.
o Bronchiole collapse: Small airways collapse during exhalation due to lack of
support.
o Diaphragm flattening: Chronic hyperinflation pushes the diaphragm downward,
making breathing less efficient.
• Effects of Emphysema on Lungs:

* What are the risk factors for emphysema?

• Smoking (Primary Cause) – Damages alveolar walls, impairs cilia function, and leads to
chronic inflammation.
• Air Pollution – Industrial fumes, dust, and smoke exposure exacerbate lung damage.
• Genetic Factors – Alpha-1 antitrypsin (AAT) deficiency (rare genetic disorder).
 • Occupational Exposure – Long-term exposure to chemicals, dust, and toxic fumes (e.g.,
construction, mining, welding).
• Secondhand Smoke Exposure – Increased risk of lung damage.
• Environmental and Genetic Risk Factors:

What protein deficiency increases the susceptibility of an individual to developing

emphysema?

-Alpha-1 Antitrypsin (AAT) Deficiency

• AAT is a protective enzyme produced in the liver that prevents lung damage from
neutrophil elastase.
• If AAT is deficient, neutrophil elastase destroys alveoli, leading to early-onset
emphysema, even in non-smokers.
• Genetic Factor:
o Autosomal recessive disorder → both parents must pass the defective gene.
o Common in younger patients (<40 years old) with no smoking history. -Effect of
AAT Deficiency on Lungs:

What enzyme balance is directly implicated in emphysema?

Neutrophil Elastase vs. Alpha-1 Antitrypsin (AAT) Imbalance
• Neutrophil elastase is an enzyme that breaks down elastin, an essential protein for
alveolar elasticity.
• AAT normally inhibits neutrophil elastase to protect the lungs.
• In AAT deficiency, neutrophil elastase becomes overactive, destroying lung
tissue, leading to emphysema.

Enzyme Imbalance in Emphysema:

What are the expected pulmonary function test results in emphysema? (See presentation)
PFT Abnormalities in Emphysema:
• ● ↓ FEV1 (Forced Expiratory Volume in 1 second) –> Impaired airflow out of the lungs.
• ● ↓ FEV1/FVC Ratio (<70%) –> Key indicator of airflow limitation.
• ● ↑ Residual Volume –> (due to air trapping)
• ● ↓ DLCO (Diffusing Capacity) —> ↓O2 exchange due to alveolar destruction
Pulmonary Function Test Abnormalities in Emphysema:

Emphysema summary:
• Pathophysiology: Alveolar destruction, air trapping, and hyperinflation —> Reduced gas
exchange (O2/CO2)
• Risk Factors: Smoking, pollution, genetic AAT deficiency, occupational exposure.
 • Protein Deficiency: Alpha-1 Antitrypsin Deficiency (AAT)→ Leads to early-onset
emphysema.
• Enzyme Imbalance: Neutrophil Elastase (too much) vs. AAT (too little) → Lung tissue
destruction.
• PFT Abnormalities: ↓ FEV1, ↓ FEV1/FVC Ratio, ↑ Residual Volume, ↓ DLCO → Poor
exhalation & oxygenation.
Quick Review
• Lung Damage – Alveolar wall destruction, leading to hyperinflation.
• Smoking Risk – Primary cause of emphysema and lung damage.
• Genetic Risk – AAT deficiency increases susceptibility.
• Pulmonary Function Test – Decreased FEV1, increased residual volume
• Enzyme Imbalance – Too much neutrophil elastase, not enough AAT → Alveolar
destruction.

ASTHMA (4 QUESTIONS)

Know the different types of asthma and the causes (see chart in recordings)

1. Allergic (Extrinsic) Asthma – Triggered by allergens like pollen, dust mites, mold, and pet
dander.

2. Non-Allergic (Intrinsic) Asthma – Triggered by non-allergic factors such as stress,

respiratory infections, strong emotions, and exposure to irritants.

3. Exercise-Induced Asthma – Symptoms occur during or immediately after physical activity,

often due to airway cooling and drying.

4. Occupational Asthma – Caused by exposure to workplace irritants, including fumes, dust,

and chemicals.

5. Nocturnal Asthma – Symptoms worsen at night, possibly due to circadian rhythms, airway
cooling, or increased exposure to allergens while lying down
 What are the roles of…

Mast cells

• Activated by allergens binding to IgE antibodies, leading to degranulation. • Release histamine,

leukotrienes, and prostaglandins, which:
• Promote bronchoconstriction.
• Increase mucus production.

• Enhance vascular permeability, contributing to airway inflammation and swelling

Eosinophils

• Attracted by interleukin-5 (IL-5), a cytokine that plays a central role in asthma inflammation. •
Release cytotoxic granules that:
• Cause tissue damage.
• Contribute to airway remodeling (long-term structural changes).

• Increase airway hyperresponsiveness and inflammation

Leukotrienes

• Potent inflammatory mediators produced by Th2 cells and mast cells.

• Functions:
• Sustain bronchoconstriction.
• Increase mucus secretion.
• Enhance airway inflammation and hyperresponsiveness.
• Important target for asthma treatments like leukotriene receptor antagonists
(e.g., Montelukast)
ACUTE RENAL FAILURE (4 QUESTIONS)

Be able to explain the pathophysiology of acute renal failure

• ARF (also called Acute Kidney Injury (AKI)).

o AKI = ARF
• This is sudden (acute), severe decline in kidney function (hours to days) ARF = FAST
• Result: build up of waste in kidneys and blood (ElevatednBUN, Creatinine) and
electrolyte imbalances.

Pathophysiology:

• When the kidneys are suddenly sick (ARF), filtration rate goes down (lower GFR)
(they’re sick, they can’t do their job— which is filtering blood. But can any of us blame
them? Of course they don’t want to work when they’re sick— no one does.).
• When the GFR goes down less waste products are filtered out (meaning we have elevated
BUN and creatinine in the blood). So there’s an inverse relationship between GFR and
BUN and Creatinine. Less filtration MEANS more waste in blood. Capiche?
• ⬆ BUN, ⬆ Creatinine in blood) Electrolytes: Elevated K and Decreased Na = metabolic
acidosis
o (Remember K+ and Na+ are inverse because they’re both positively charged— if
one I out of range on their higher end, the other will be out of range on their lower
end)

Know the stages of acute renal failure/AKI and what happens in each stage including
changes in fluids and electrolytes, Know the risk factors and causes of each stage
 • ● Initial phase = mild or none electrolyte imbalance, no retention
• ● Oliguric phase = retention (elevated K+, fluid overload)
• ● Diuretic phase = excessive urine output (risk for dehydration)

What are the different TYPES of acute renal failure?

What is pre-renal acute renal failure?
• Something in the body causes decreased blood flow to the kidneys (usually decreased
cardiac output, hypovolemia, dehydration, etc). There’s not a KIDNEY problem, there’s
a BLOOD FLOW problem BEFORE the kidneys. This causes Oliguria (low urine
output), because the kidneys try to retain water to increase the blood volume.
• Key Causes:
o ● Hypovolemia (severe dehydration, hemorrhage)
o ● Heart failure (low cardiac output)
o ● Septic shock/burn
 •
• Lab Findings for Pre-renal ARF: urine output <400mL/day (oliguria)
o ● BUN/Creatinine ratio higher than 20:1
o ● Urine Na+ less than 20 mEq/L (kidneys trying to retain Na+)
What is intrinsic (intra-renal) acute renal failure?
• This one is a KIDNEY PROBLEM. There’s injury to kidney structures: glomeruli,
tubules, or interstitium (spaces in between essential kidney structures). If severe, this can
be irreversible.
• Key Causes:
o ● Nephrotoxic drugs (NSAIDs, aminoglycosides, contrast dye)
o ● Acute tubular necrosis (ATN)
o ● Glomerulonephritis
o ● Autoimmune diseases (lupus, vasculitis)
• Lab Findings for Intrinsic ARF:
o ● BUN/Creatinine ratio <15:1
o ● Urine sodium >40 mEq/L (kidneys can’t retain Na+ properly)
o ● Muddy brown casts in urine (ATN)
What is post-renal acute renal failure?
• Caused by OBSTRUCTION of urine flowing OUT of kidneys. This puts pressure of fluid
BACK into the kidneys, causing hydronephrosis
• Key Causes:
o ● Kidney stones
o ● Prostate enlargement (BPH)
o ● Bladder outlet obstruction (tumors, strictures)
 • Lab Findings for Post-renal ARF:
o ● Variable BUN/Creatinine ratio
o ● Hydronephrosis on imaging (ultrasound, CT scan
Who is at risk for acute renal failure?

PNEUMONIA (3-4 QUESTIONS)

Difference between bacterial and viral pneumonia

Bacterial Viral
Causes: viruses like influenza, respiratory
Causes: Strong neutrophil response, most syncytial virus (RSV), coronaviruses (e.g.,
commonly Streptococcus pneumoniae, COVID-19), and others.
Haemophilus influenzae, and Mycoplasma
pneumoniae. Onset: develops more gradually, often
following a cold or the flu.
Onset: tend to come on suddenly and can be
more severe Symptoms: dry cough, fever, body aches,
fatigue, and sometimes shortness of breath.
Symptoms: high fever, chills, chest pain,
productive cough (with mucus or phlegm), and Treatment: cannot be treated with antibiotics.
difficulty breathing. Treatment focuses on supportive care, such as
rest, hydration, and antiviral medications
Treatment: treated with antibiotics. The choice Complications: can lead to secondary
of antibiotic depends on the type of bacteria bacterial infections
causing the infection.

Complications: atelectasis, pleural effusion

(fluid around the lungs), lung abscesses, and
septic shock. Severe and long term cases =
fibrosis

What happens at the alveolar level due to inflammation

• Alveolar and Capillary Changes

o Fluid and Cellular Exudate - Increased capillary permeability allows fluid,
proteins, and immune cells to fill the alveoli
o Alveolar Consolidation - fluid and cellular debris create a dense,
consolidated appearance in affected lung areas
o Impaired Gas Exchange - accumulation of fluid disrupts normal oxygen and
carbon dioxide exchange

Recognize the compensatory response to hypoxemia

• Lungs will initiate hyperventilation in order to obtain more oxygen for blood gas
exchange and adequate perfusion. The problems are....
o Respiratory fatigue from trying to maintain high breathing rates. Can create
opportunity for further respiratory acidosis (CO2 is not being eliminated
sufficiently either) furthering sepsis potential.
o Cardiac overload from increased heart rate and output, potentially leading to
heart failure.
o Pulmonary hypertension caused by chronic vasoconstriction in the lungs,
putting additional stress on the right side of the heart. Lungs will constrict
vessels in poorly perfused areas to shunt/redirect that blood flow and increase
 perfusion to adequately perfused areas in an effort to maintain or increase
blood gas exchange and oxygen obtainment
o Organ damage due to reduced blood flow to non-vital areas from shunting
from from areas such as digestive and skin toward more vital organs (heart,
lungs, brain) to maintain perfusion
• Overall can lead to multi organ failure if not treated and compensatory mechanisms
fail.

TB (3-4 QUESTIONS)

What type of hypersensitivity reaction is responsible for the formation of

granulomas associated with TB? A-C-I-D :)
• Delayed or Cell Mediated.

Which immune cells play a main role in isolating the TB mycobacterium in the
lunges?
• Consists of macrophages, T cells, B cells, and other immune cells; and they surround the
infected cells.

What causes the cavitation in the lungs?

• Damaged lung tissue has been destroyed (necrosis), creating hollow areas where air
can collect.

NOTES FROM AMANDA

chronic bronchitis (ppt and exam review)
emphysema vs bronchitis
RAAS
anatomy of nephron and where things are absorbed and excreted
if its connected to something else, know that too
what part of loop of Henle is not permeable to water (ascending)
most is absorbed into proximal
in terms of anatomy… know how RAAS affects certain parts of nephron
how does angiotensin 2 affect GFR?? (vasoconstriction) it increases it (more blood to
kidneys = higher GFR)
efferent right before tubule
afferent, leading into glomerulus
CALCIUM AND PHOSPHATE HAVE INVERSE RELATIONSHIP
intra: woman in the cell “im going to Kickyour (potassium) MAGA (magnesium) ass off my
Patio (phosphate) Pronto (protein)
extra: NA (sodium) Chill (chlorine) youre BIased (bicarb)
renal:
Know different faces of AKI
(oligeric phase, lab values)
distal tubule produces parathyroid horomone will reabsorb calcium and potassium and
where aldosterone works
collecting duct is where ADH works
loop of henle is where water and a lot of different solutes are released

loop of henle, distal tubule and proximal tubule ****

listen to exam review

why would someone with CKD be anemic… THEY DONT PRODUCE

ERYTHROPOEITIN
CKD… know ABG (metabolic acidosis) thye cant excrete H and K and BICARB and
Phosphorus (which reduces calcium)
if you retain sodium in a normal kidney, you will exrete K (aldosterone retains sodium and
water)
Pancreatitis…phosphorus binds with free calcium
phosphorus binds to free calcium
sodium and pot inverse
water and sodium
hco3 and co2- frienamies

RAAS
Renin to angiotensin: renin acts on angiotensinegin (produced by liver), liver releases into
blood stree, where kidney cuts it in half and angiotensin 1 is born. it then goes to lungs,
parties with ACE and creates angiotensin 2. angiotenin 2 has party in efferent glomerulus
and causes systemic vasocontricition. aldosterone in distal tubule retains sodium and water
and secretes potassium which in turn raises BP

emphysema… alpha

ARF
fast and sudden (hours to days)
can cause issues because kidneys are
GFR LOW (
BUN AND CREAT INCREASED
3 types
pre-renal- something happeneing before kidneys (hypovolemia, burns,
dehydration,hemmorhage)
LABS: bun/creat>20:1, urine sodium <20
intrinsic- something happening within the kidneys (direct damage on kidney ie sepsis/
structural damage), can be irreversable
LABS: BUN/Cret<15:1, muddy brown casts
post-renal- something happening after kidneys (urine flow obstruction), back pressure,
LABS: hydronephrosis on imaging (CT and US)
diabetics, HF and elderly, NSAIDS and immunoglycosides, sepsis

4 stages (normal is 500-900)

1. initial- normal electolytes
 2. oliguric (decreased urin >400) fluid overload increased bp and edema, holding K
and low Na
3. diuretic-poluuria (3-5 l per day), dehydration, low K and NA
4. recovery- starts to balance out

chronic bronchitis (a COPD)

bronchitis
macrophages and neutrophils & killer cells
airway remodeling due to chronic inflamation (chronic resp. infections)
goblet cells (theres more, to try to compensate)—more mucus secretion
decreased cillia (cant move things out)-damaged more by smoking and polutants
(blue bloaters)
air trapping
KNOW HOW TOTAL VOLUME CAPASITY CHANGES AND RESIDUAL CAPASITY
CHANGES
-decreased
-increased

eMPHYSEMA
-damage to alveoli (terminal end to lung cells)
decreased elastisity-leading to collapsed bronchille tree
-decreased expiration
-poor gas exchange
-(pink puffer) barrel chest, tripoding, anxious state, skinny
KNOW HOW TOTAL VOLUME CAPASITY CHANGES AND RESIDUAL CAPASITY
CHANGES
-Increased in both
-air trapping (worse)
-SEPTA BREAKS DOWN, ONLY SURFACE AREA THEY HAVE
RISKS: smoking and air polution, AAT abnormality (rare genetic disorder)-works to
combat neutrophil elastase (enzyme that breaks down elastin) which causes an imbalanced,
KNOW WHAT ENZYME IMBALANCE IS KEY (Antiproteazis and proteazis)