review Flashcards

1
Q
  1. Signs/Symptoms of RA vs OA?
    - joint deformity
    - joint tenderness
    - decreased ROM
    - herbedens nodes – distal finger (interphalangeal) joints crooked
    - bouchards nodes – proximal finger (interphalangeal) joints are crooked
A

B- joint deformity
B- joint tenderness
B- decreased ROM
OA- herbedens nodes – distal finger (interphalangeal) joints crooked
OA- bouchards nodes – proximal finger (interphalangeal) joints are crooked

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2
Q
  1. Relationship between alcoholism and liver disease
    - Excessive alcohol consumption is a leading cause of liver ________ and increases the risk of liver ________
    - Alcoholic liver disease ranges from _______ liver to life-threatening ________ and liver failure.
    - Alcohol is metabolized into acetaldehyde, which is _______ to liver cells and activates inflammatory pathways.
    - Chronic alcohol exposure leads to:
    o ____ accumulation (steatosis),
    o inflammation (alcoholic _________)
    o progressive ________ (cirrhosis) in the liver.
A
  1. Relationship between alcoholism and liver disease
    - Excessive alcohol consumption is a leading cause of liver disease and increases the risk of liver cancer.
    - Alcoholic liver disease ranges from fatty liver to life-threatening cirrhosis and liver failure.
    - Alcohol is metabolized into acetaldehyde, which is toxic to liver cells and activates inflammatory pathways.
    - Chronic alcohol exposure leads to:
    o fat accumulation (steatosis),
    o inflammation (alcoholic hepatitis)
    o progressive scarring (cirrhosis) in the liver.
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3
Q

thyroid, hypothalamus, pituitary, hashimoto’s

Primary hypothyroidism -
_____ levels (T3 and T4) with ____ levels of (TSH)
Secondary hypothyroidism -
_____ levels of T3, T4, and TSH2.
Tertiary hypothyroidism -
_____ levels of T3, T4, TSH, and TRH3.
Autoimmune disorders -
_____ T3 and T4 and _____ TSH1.

A

Primary hypothyroidism - thyroid
Low levels (T3 and T4) with high levels of (TSH)
Secondary hypothyroidism - pituitary
Low levels of T3, T4, and TSH2.
Tertiary hypothyroidism - hypothalamus
Low levels of T3, T4, TSH, and TRH3.
Autoimmune disorders - hashimoto’s
low T3 and T4 and high TSH1.

thyroid secretes - T3 and T4
Hypothalamic-pituitary secretes - TSH

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4
Q

So with right sided heart failure = s/s blood backs up in _________ circulation
- Congestion in right chambers
- Right ventricle size increase
- Backflow into vena cava, decreased blood to the lungs
- Congestion in jugular veins, liver, lower extremities (body)
- Common cause – COPD

Findings:
- JVD
- Dependent/Peripheral edema – lower extremities
- Weight gain
- Hepatosplenomegaly – enlarged spleen/liver
- Ascites (fluid accumulation in abdomen)
- Nausea, anorexia

A

So with right sided heart failure = s/s blood backs up in systemic circulation
- Congestion in right chambers
- Right ventricle size increase
- Backflow into vena cava, decreased blood to the lungs
- Congestion in jugular veins, liver, lower extremities (body)
- Common cause – COPD
Findings:
- JVD
- Dependent/Peripheral edema – lower extremities
- Weight gain
- Hepatosplenomegaly – enlarged spleen/liver
- Ascites (fluid accumulation in abdomen)
- Nausea, anorexia

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5
Q

Secondary Hypothyroidism:

Cause: Dysfunction of the pituitary gland, which fails to produce enough TSH to stimulate the thyroid.

Hormone Levels: _____ levels of T3, T4, and TSH2.

Common Causes: Pituitary tumors, radiation therapy, or pituitary surgery.

A

Secondary Hypothyroidism:
Cause: Dysfunction of the pituitary gland, which fails to produce enough TSH to stimulate the thyroid.
Hormone Levels: Low levels of T3, T4, and TSH2.
Common Causes: Pituitary tumors, radiation therapy, or pituitary surgery.

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6
Q

Tertiary Hypothyroidism:

Cause: Dysfunction of the hypothalamus, which fails to produce enough thyrotropin-releasing hormone (TRH) to stimulate the pituitary gland.

Hormone Levels: ______ levels of T3, T4, TSH, and TRH3

Common Causes: Hypothalamic tumors, trauma, or radiation therapy affecting the hypothalamus3.

A

Tertiary Hypothyroidism:

Cause: Dysfunction of the hypothalamus, which fails to produce enough thyrotropin-releasing hormone (TRH) to stimulate the pituitary gland.
Hormone Levels: Low levels of T3, T4, TSH, and TRH3.
Common Causes: Hypothalamic tumors, trauma, or radiation therapy affecting the hypothalamus3.

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7
Q
  1. Onset/duration of Insulins
    ________-acting (lispro, aspart, glulisine):
    Onset: 10-30 minutes
    Peak: 30 minutes - 3 hours
    Duration: 3-5 hours

_______-acting (regular):
Onset: 30 minutes - 1 hour
Peak: 2-5 hours
Duration: 5-8 hours

__________-acting (NPH):
Onset: 1.5-4 hours
Peak: 4-12 hours
Duration: 12-18 hours

________-acting (glargine, detemir, degludec):
Onset: 0.8-4 hours
Peak: Less defined or no pronounced peak
Duration: 16-24 hours

A
  1. Onset/duration of Insulins
    Rapid-acting (lispro, aspart, glulisine):
    Onset: 10-30 minutes
    Peak: 30 minutes - 3 hours
    Duration: 3-5 hours

Short-acting (regular):
Onset: 30 minutes - 1 hour
Peak: 2-5 hours
Duration: 5-8 hours

Intermediate-acting (NPH):
Onset: 1.5-4 hours
Peak: 4-12 hours
Duration: 12-18 hours

Long-acting (glargine, detemir, degludec):
Onset: 0.8-4 hours
Peak: Less defined or no pronounced peak
Duration: 16-24 hours

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8
Q
  1. Complications of poorly controlled DM

Acute or chronic complications?
- Hypoglycemia (low blood sugar)
- Diabetic ketoacidosis (DKA)
- Hyperosmolar hyperglycemic state
- Macrovascular: Coronary artery disease,
- Macrovascular: peripheral vascular disease,
- Macrovascular: stroke
- Microvascular: Retinopathy,
- Microvascular: nephropathy,
- Microvascular: neuropathy

A

Acute Complications:
- Hypoglycemia (low blood sugar)
- Diabetic ketoacidosis (DKA)
- Hyperosmolar hyperglycemic state

Chronic Complications:
- Macrovascular: Coronary artery disease, peripheral vascular disease, stroke
- Microvascular: Retinopathy, nephropathy, neuropathy

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9
Q

Basic DM pathophysiology
1. Insulin is a hormone produced by the ____________ beta cells that regulates blood glucose levels.
2. there is either insufficient insulin production (type ___) or the body’s cells are resistant to insulin’s effects (type ___), leading to hyperglycemia.
3. Chronic hyperglycemia causes cellular _____ and metabolic abnormalities affecting various organs.
4. In type 1 diabetes, the ________ attacks and destroys the insulin-producing beta cells.
5. In type 2 diabetes, insulin ______ and relative insulin ________ occur due to factors like obesity, sedentary lifestyle, and genetic predisposition.

A
  1. Insulin is a hormone produced by the pancreatic beta cells that regulates blood glucose levels.
  2. there is either insufficient insulin production (type 1) or the body’s cells are resistant to insulin’s effects (type 2), leading to hyperglycemia.
  3. Chronic hyperglycemia causes cellular damage and metabolic abnormalities affecting various organs.
  4. In type 1 diabetes, the body’s immune system attacks and destroys the insulin-producing beta cells.
  5. In type 2 diabetes, insulin resistance and relative insulin deficiency occur due to factors like obesity, sedentary lifestyle, and genetic predisposition.
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10
Q

So with left sided heart failure = s/s blood backs up in ________ circulation
- Congestion in left chambers
- Left ventricle size increase
- Backflow into pulmonary veins
- Congestion in lungs
- Common cause – HTN

Findings:
- Cough, crackles, wheezes
- Pulmonary edema – frothy sputum, blood tinged
- Paroxysmal nocturnal dyspnea (PND) – feel smothered at night, waking up suddenly gasping for air
- Shortness of breath
- orthopnea (difficulty breathing while lying flat) – tripod to breathe best
- Fatigue, confusion due to low cardiac output

A

So with left sided heart failure = s/s blood backs up in pulmonary circulation
- Congestion in left chambers
- Left ventricle size increase
- Backflow into pulmonary veins
- Congestion in lungs
- Common cause – HTN
Findings:
- Cough, crackles, wheezes
- Pulmonary edema – frothy sputum, blood tinged
- Paroxysmal nocturnal dyspnea (PND) – feel smothered at night, waking up suddenly gasping for air
- Shortness of breath
- orthopnea (difficulty breathing while lying flat) – tripod to breathe best
- Fatigue, confusion due to low cardiac output

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11
Q
  1. Expected findings of iron deficiency anemia
    - ____ hemoglobin and hematocrit levels
    - ______cytic and _____chromic red blood cells
    - _____ mean corpuscular volume (MCV) and ______ mean corpuscular hemoglobin concentration (MCHC)
    - ______ serum ferritin and transferrin saturation levels
    - Potential symptoms like fatigue, weakness, pallor, headaches, ______ cravings
    - Physical signs like _________ (spoon nails), _______itis, angular ______titis
    - In children, poor growth, irritability, developmental delays
A
  1. Expected findings of iron deficiency anemia
    - Low hemoglobin and hematocrit levels
    - Microcytic (small) and hypochromic (pale) red blood cells
    - Low mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC)
    - Low serum ferritin and transferrin saturation levels
    - Potential symptoms like fatigue, weakness, pallor, headaches, pica cravings
    - Physical signs like koilonychia (spoon nails), glossitis, angular stomatitis
    - In children, poor growth, irritability, developmental delays
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12
Q
  1. HTN medications:

Beta Blockers:
Common side effects –
- ______cardia,
- hyp___tension,
- fatigue,
- bronchospasm (non-selective agents)
Hold for -
- bradycardia,
- heart block,
- decompensated heart failure,
- reactive airway disease exacerbation

ACE Inhibitors:
Common side effects –
- c______
- hyp___tension,
- hyp___kalemia,
- angioedema,
- acute kidney injury
Hold for –
- angioedema,
- severe hypotension,
- hyperkalemia,
- acute kidney injury

ARBs:
Common side effects –
- Hyp___tension,
- hyp___kalemia,
- dizziness
Hold for –
- severe hypotension,
- hyperkalemia,
- acute kidney injury

Calcium Channel Blockers:
Common side effects –
- Peripheral edema,
- headache,
- flushing,
- constipation
Hold for –
- severe hypotension,
- bradycardia,
- heart block

A
  1. HTN medications: Beta blockers, ACE inhibitors, ARBS, CCB. Common side effects and when to hold.
    Beta Blockers:
    Common side effects –
    - Bradycardia,
    - hypotension,
    - fatigue,
    - bronchospasm (non-selective agents)
    Hold for -
    - bradycardia,
    - heart block,
    - decompensated heart failure,
    - reactive airway disease exacerbation

ACE Inhibitors:
Common side effects –
- Cough,
- hypotension,
- hyperkalemia,
- angioedema,
- acute kidney injury
Hold for –
- angioedema,
- severe hypotension,
- hyperkalemia,
- acute kidney injury

ARBs:
Common side effects –
- Hypotension,
- hyperkalemia,
- dizziness
Hold for –
- severe hypotension,
- hyperkalemia,
- acute kidney injury

Calcium Channel Blockers:
Common side effects –
- Peripheral edema,
- headache,
- flushing,
- constipation
Hold for –
- severe hypotension,
- bradycardia,
- heart block

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13
Q
  1. Signs/Symptoms of RA vs OA?
    - Manifestations are asymmetrical
    - Manifestations are symmetrical
    - deep aching joint pain – esp with exertion, relieved with rest
    - joint pain with cold weather
    - stiffness in morning
    - crepitus of joint during motion
    - joint swelling – hard
    - joint swelling - spongy warm
    - altered gait
    - limited range of motion
A

OA - Manifestations are asymmetrical
RA - Manifestations are symmetrical
OA - deep aching joint pain – esp with exertion, relieved with rest
OA- joint pain with cold weather
OA- stiffness in morning
OA- crepitus of joint during motion
OA- joint swelling – hard
RA - joint swelling - spongy warm
OA- altered gait
OA- limited range of motion

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14
Q
  1. Symptoms of different diseases that fall under COPD

____________
- Persistent cough with mucus production
- Wheezing
- Shortness of breath, especially with activity

_____________
- Shortness of breath, initially with exertion
- Wheezing
- Chest tightness
- Frequent respiratory infections

_____________
- Progressive dyspnea (shortness of breath)
- Chronic cough
- Sputum production
- Fatigue
- Pursed-lip breathing
- Use of accessory muscles for breathing
- Barrel-chested appearance in advanced stages

A
  1. Symptoms of different diseases that fall under COPD

Chronic bronchitis:
- Persistent cough with mucus production
- Wheezing
- Shortness of breath, especially with activity

Emphysema:
- Shortness of breath, initially with exertion
- Wheezing
- Chest tightness
- Frequent respiratory infections

General COPD symptoms:
- Progressive dyspnea (shortness of breath)
- Chronic cough
- Sputum production
- Fatigue
- Pursed-lip breathing
- Use of accessory muscles for breathing
- Barrel-chested appearance in advanced stages

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15
Q
  1. Complications of acute viral gastroenteritis?
    - __________ : Excessive fluid loss from vomiting and diarrhea
    - ___________ Imbalances: from GI loss, can result in metabolic acidosis and dysrhythmias if not corrected.
    -__________: Prolonged GI loss, impair nutrient absorption, vitamin/mineral deficiencies and weight loss
    - Intestinal Complications: Severe inflammation can lead to complications like toxic ________, intestinal __________, or intussusception (telescoping of intestines).
    - __________ Complications: Dehydration and electrolyte disturbances may rarely cause seizures, encephalopathy, or Guillain-Barré syndrome.
    - Renal Complications: Dehydration and electrolyte abnormalities increase the risk of ________ kidney injury or hemolytic uremic syndrome in some cases.
A
  • Dehydration: Excessive fluid loss from vomiting and diarrhea
  • Electrolyte Imbalances: from GI loss, can result in metabolic acidosis and dysrhythmias if not corrected.
  • Malnutrition: Prolonged GI loss, impair nutrient absorption, vitamin/mineral deficiencies and weight loss
  • Intestinal Complications: Severe inflammation can lead to complications like toxic megacolon, intestinal perforation, or intussusception (telescoping of intestines).
  • Neurological Complications: Dehydration and electrolyte disturbances may rarely cause seizures, encephalopathy, or Guillain-Barré syndrome.
  • Renal Complications: Dehydration and electrolyte abnormalities increase the risk of acute kidney injury or hemolytic uremic syndrome in some cases.
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16
Q
  1. Basic causes of cancer
    Cancer arises from accumulated genetic mutations that allow cells to escape normal growth controls and become malignant.

The main causes include:
- ____________ exposures like tobacco smoke, UV radiation, and carcinogenic chemicals. These can directly damage DNA or generate reactive molecules that cause mutations.
- __________ mutations in oncogenes or tumor suppressor genes that increase cancer susceptibility.
- Random mutations from errors during normal cell __________ and metabolism. As we ____, mutations accumulate.
- Chronic _________ which generates mutagenic molecules and growth factors that promote tumor development.
- ______ infections like human papillomavirus (HPV), hepatitis B/C viruses which can integrate viral genes or induce mutations.
- _______ imbalances, like excess estrogen exposure linked to certain breast cancers.

A
  1. Basic causes of cancer
    Cancer arises from accumulated genetic mutations that allow cells to escape normal growth controls and become malignant.

The main causes include:
- Environmental exposures like tobacco smoke, UV radiation, and carcinogenic chemicals. These can directly damage DNA or generate reactive molecules that cause mutations.
- Inherited genetic mutations in oncogenes or tumor suppressor genes that increase cancer susceptibility. About 5-10% of cancers are hereditary.
- Random mutations from errors during normal cell replication and metabolism. As we age, mutations accumulate.
- Chronic inflammation which generates mutagenic molecules and growth factors that promote tumor development.
- Viral infections like human papillomavirus (HPV), hepatitis B/C viruses which can integrate viral genes or induce mutations.
- Hormonal imbalances, like excess estrogen exposure linked to certain breast cancers.

17
Q
  1. Basic adverse effects of cancer chemotherapeutic agents
  • pancytopenia - _____, ______, _______
  • GI issues
  • Alopecia (hair loss)
  • Fatigue
  • Increased ___________ risk
  • Organ toxicities (nephrotoxicity, cardiotoxicity, hepatotoxicity, etc.)
  • Peripheral neuropathy
  • Infertility
  • Secondary malignancies
A
  1. Basic adverse effects of cancer chemotherapeutic agents
  • pancytopenia - Myelosuppression (decreased blood cell counts leading to anemia, neutropenia, thrombocytopenia)
  • Gastrointestinal toxicity (nausea, vomiting, diarrhea, mucositis)
  • Alopecia (hair loss)
  • Fatigue
  • Increased infection risk
  • Organ toxicities (nephrotoxicity, cardiotoxicity, hepatotoxicity, etc.)
  • Peripheral neuropathy
  • Infertility
  • Secondary malignancies
18
Q

Autoimmune Hypothyroidism:

Cause: The immune system attacks the thyroid gland, leading to its dysfunction.

Hormone Levels: Typically presents as primary hypothyroidism with ____ T3 and T4 and ____ TSH1.

Common Causes: Hashimoto’s thyroiditis is the most common form of autoimmune hypothyroidism

A

Autoimmune Hypothyroidism:
Cause: The immune system attacks the thyroid gland, leading to its dysfunction.
Hormone Levels: Typically presents as primary hypothyroidism with low T3 and T4 and high TSH1.
Common Causes: Hashimoto’s thyroiditis is the most common form of autoimmune hypothyroidism

19
Q

Medications for HF (and the contraindications for giving them)
1.- ___________: (e.g. lisinopril, enalapril)
Contraindicated in pregnancy, angioedema (life-threatening allergic reaction causing swelling of the face, lips, tongue, and airways), hyperkalemia.
2.- ___________: (e.g. valsartan, losartan)
Contraindicated in pregnancy, renal artery stenosis, hyperkalemia.
3.- Valsartan/Sacubitril: (Entresto)
Contraindicated in pregnancy, history of angioedema.
4.- Beta Blockers: (e.g. carvedilol, metoprolol)
Contraindicated in _____cardia, heart blocks, decompensated HF.
5.- Aldosterone Antagonists: (e.g. ________)
Contraindicated in hyperkalemia, renal impairment.
6.- ___________: (e.g. furosemide)
Contraindicated in anuria, hepatic coma.
7.- Digoxin
Contraindicated in ventricular fibrillation, Wolff-Parkinson-White syndrome.
8.- Hydralazine/Isosorbide Dinitrate
Contraindicated in coronary artery disease, tachycardia.

A

1.- ACE Inhibitors: (e.g. lisinopril, enalapril)
Contraindicated in pregnancy, angioedema (life-threatening allergic reaction causing swelling of the face, lips, tongue, and airways), hyperkalemia.
2.- Angiotensin II Receptor Blockers (ARBs): (e.g. valsartan, losartan)
Contraindicated in pregnancy, renal artery stenosis, hyperkalemia.
3.- Valsartan/Sacubitril: (Entresto)
Contraindicated in pregnancy, history of angioedema.
4.- Beta Blockers: (e.g. carvedilol, metoprolol)
Contraindicated in bradycardia, heart blocks, decompensated HF.
5.- Aldosterone Antagonists: (e.g. spironolactone, eplerenone)
Contraindicated in hyperkalemia, renal impairment.
6.- Loop Diuretics: (e.g. furosemide)
Contraindicated in anuria, hepatic coma.
7.- Digoxin
Contraindicated in ventricular fibrillation, Wolff-Parkinson-White syndrome.
8.- Hydralazine/Isosorbide Dinitrate
Contraindicated in coronary artery disease, tachycardia.

20
Q
  1. Signs/Symptoms of RA vs OA?
  • Early - Very little s/s, Maybe joint pain
  • Inflammation
  • Heat
  • Joint subluxation
  • Fatigue and malaise
  • Could affect any and all body systems if severe enough
  • SJORGRENS SYNDROME – destruction of moisture producing gland (salivary and lacrimal) – dry mouth and eyes
  • Rheumatoid nodules – immune mediated granulomas, develop around inflamed joints, SQ and firm, maybe painful
A

RA- Early - Very little s/s, Maybe joint pain
RA- Inflammation
RA- Heat
RA- Joint subluxation
RA- Fatigue and malaise
RA- Could affect any and all body systems if severe enough
RA- SJORGRENS SYNDROME – destruction of moisture producing gland (salivary and lacrimal) – dry mouth and eyes
RA- Rheumatoid nodules – immune mediated granulomas, develop around inflamed joints, SQ and firm, maybe painful

21
Q

```

Primary Hypothyroidism:

Cause: Direct dysfunction of the thyroid gland itself.

Hormone Levels: _____ levels of thyroid hormones (T3 and T4) with ____ levels of thyroid-stimulating hormone (TSH) due to the pituitary gland trying to stimulate the thyroid.

Common Causes: thyroiditis, congenital hypothyroidism, surgical removal of the thyroid, or radiation to thyroid.

A

Primary Hypothyroidism:
Cause: Direct dysfunction of the thyroid gland itself.
Hormone Levels: Low levels of thyroid hormones (T3 and T4) with high levels of thyroid-stimulating hormone (TSH) due to the pituitary gland trying to stimulate the thyroid.
Common Causes: thyroiditis, congenital hypothyroidism, surgical removal of the thyroid, or radiation to thyroid.

22
Q
  1. MOA of PUD medications
  2. Antacids
    MOA - Neutralizes _____
  3. Cimetidine and Famotidine: ____ receptor antagonists
    MOA
    - target gastric acid production
    - Block _____ receptors in the stomach
    - Reduce gastric acid secretion
    - ___creases stomach pH
  4. Omeprazole, Pantoprazole, Esomeprazole magnesium: _________
    MOA
    – target gastric acid production
    - Binds to _________
    - Inhibits the hydrogen potassium ATPase enzyme system (proton pump)
  5. Sucralfate: protectants
    MOA
    - Forms a protective barrier over ulcers by binding to exposed proteins.
    - Also stimulates mucosal defense factors like bicarbonate and prostaglandins.
  6. Misoprostol: prostaglandin analog.
    MOA
    - A prostaglandin analog that enhances mucosal defense by increasing mucus and bicarbonate secretion while reducing acid secretion.
  7. Antibiotics (e.g. amoxicillin, clarithromycin)
    MOA
    - Used in combination to eradicate H. pylori infection, a major cause of PUD.
A
  1. Antacids
    MOA - Neutralizes acid
  2. Cimetidine and Famotidine: H2 receptor antagonists
    MOA
    - target gastric acid production
    - Block h2 recpetors in the stomach
    - Reduce gastric acid secretion
    - Increases stomach pH
  3. Omeprazole, Pantoprazole, Esomeprazole magnesium: Proton pump inhibitors (PPI)
    MOA
    – target gastric acid production
    - Binds to proton pump
    - Inhibits the hydrogen potassium ATPase enzyme system (proton pump)
  4. Sucralfate:
    MOA
    - Forms a protective barrier over ulcers by binding to exposed proteins.
    - Also stimulates mucosal defense factors like bicarbonate and prostaglandins.
  5. Misoprostol:
    MOA
    - A prostaglandin analog that enhances mucosal defense by increasing mucus and bicarbonate secretion while reducing acid secretion.
  6. Antibiotics (e.g. amoxicillin, clarithromycin)
    MOA
    - Used in combination to eradicate H. pylori infection, a major cause of PUD.
23
Q

Inhaled corticosteroids are:
- designed for direct delivery to the lungs to treat respiratory conditions like _____ and ________
- They have a more _______ effect with minimal _______ absorption at standard doses.
- Inhaled steroids have _______ overall side effects compared to systemic steroids
- high doses of inhaled steroids can still lead to some systemic absorption and adverse effects.

Systemic corticosteroids:
- Ex: prednisone
- taken orally or injected, leading to ______ distribution throughout the body.
- They are used for various __________ and _________ disorders.
- Have _______ overall side effects compared to inhaled steroids
- can cause adrenal ________, immuno_________, fluid/electrolyte disturbances, and metabolic effects with long-term use.

A

Inhaled corticosteroids are
- designed for direct delivery to the lungs to treat respiratory conditions like asthma and COPD.
- They have a more localized effect with minimal systemic absorption at standard doses.
- Inhaled steroids have fewer overall side effects compared to systemic steroids
- high doses of inhaled steroids can still lead to some systemic absorption and adverse effects.
Systemic corticosteroids
- Ex: prednisone
- taken orally or injected, leading to widespread distribution throughout the body.
- They are used for various inflammatory and autoimmune disorders.
- Have more overall side effects compared to inhaled steroids - which can cause adrenal suppression, immunosuppression, fluid/electrolyte disturbances, and metabolic effects with long-term use.

24
Q

___________ hypothyroidism - originates from the hypothalamus with decreased TRH production, leading to reduced TSH and thyroid hormones.

___________ hypothyroidism - stems from an abnormality in the thyroid gland itself, such as the inability to release thyroid hormones or defects in hormone synthesis.

______________ hypothyroidism- Hashimoto’s thyroiditis, where the body attacks its own thyroid tissue, can also cause hypothyroidism.

____________ hypothyroidism - begins at the pituitary level with reduced TSH secretion.

A

Tertiary hypothyroidism - originates from the hypothalamus with decreased TRH production, leading to reduced TSH and thyroid hormones.

Primary hypothyroidism - stems from an abnormality in the thyroid gland itself, such as the inability to release thyroid hormones or defects in hormone synthesis.

Autoimmune disorders - Hashimoto’s thyroiditis, where the body attacks its own thyroid tissue, can also cause hypothyroidism.

Secondary hypothyroidism - begins at the pituitary level with reduced TSH secretion.

25
Q

PaCO2 (partial pressure of carbon dioxide)
_____ PaCO2 indicates hypoventilation/respiratory acidosis.
____ PaCO2 suggests hyperventilation/respiratory alkalosis.

HCO3- (bicarbonate)
_____ levels suggest metabolic alkalosis,
_____ levels metabolic acidosis.

A

PaCO2 (partial pressure of carbon dioxide)
High PaCO2 indicates hypoventilation/respiratory acidosis.
Low PaCO2 suggests hyperventilation/respiratory alkalosis.

HCO3- (bicarbonate)
High levels suggest metabolic alkalosis,
low levels metabolic acidosis.

26
Q
  1. Main causes of CKD
    - ___________
    - ___________
    -____________ (inflammation of kidney filters)
    - Polycystic kidney disease
    - ___________ uropathy (blockage of urine flow)
    - Recurrent kidney _________/pyelonephritis
    - Prolonged use of_________medications
A
  1. Main causes of CKD
    - Diabetes (diabetic nephropathy)
    - Hypertension
    - Glomerulonephritis (inflammation of kidney filters)
    - Polycystic kidney disease
    - Obstructive uropathy (blockage of urine flow)
    - Recurrent kidney infection/pyelonephritis
    - Prolonged use of nephrotoxic medications
27
Q

For IV heparin therapy, the key lab to monitor is the __________

Signs and symptoms to monitor include:
- B_______
- B_______
- Hematoma formation
- Hyp____tension
- Back pain (potential retroperitoneal bleed)

administering _____________ to reverse its effects if needed.

A

For IV heparin therapy, the key lab to monitor is the activated partial thromboplastin time (aPTT). It is typically checked every 6 hours until therapeutic levels are achieved.

Signs and symptoms to monitor include:
- Bleeding (nosebleeds, bleeding gums, hematuria, etc.)
- Bruising
- Hematoma formation
- Hypotension
- Back pain (potential retroperitoneal bleed)

Strict monitoring is crucial as heparin has a high risk of bleeding complications. Any concerning signs of bleeding should prompt holding the heparin infusion and administering protamine sulfate to reverse its effects if needed.

28
Q

HIV is a retrovirus that attacks the body’s immune system, specifically the _____ and helper___ cells

The basic pathophysiology involves the following steps:
1. HIV binds to the _____ receptor and a co-receptor on the host cell’s surface, allowing fusion and entry into the cell.
2. Once inside, HIV uses the enzyme ______________ to convert its RNA into DNA.
3. The viral DNA then integrates into the host cell’s genome with the help of the __________ enzyme.
4. The integrated viral DNA hijacks the host cell’s _________ to produce new viral RNA, proteins, and enzymes like protease.
5. These components assemble into new virus particles that bud off from the host cell, releasing mature virions capable of __________ other cells.
6. As HIV replicates, it progressively destroys ______ and _____ cells, impairing the immune system’s ability to fight infections and diseases.
7. The gradual depletion of CD4+ T cells leads to the development of _______ the most severe stage of HIV infection, characterized by _________ infections and cancers.

A

HIV (Human Immunodeficiency Virus) is a retrovirus that attacks the body’s immune system, specifically the CD4+ T cells (helper T cells). The basic pathophysiology involves the following steps:
1. HIV binds to the CD4 receptor and a co-receptor on the host cell’s surface, allowing fusion and entry into the cell.
2. Once inside, HIV uses the enzyme reverse transcriptase to convert its RNA into DNA.
3. The viral DNA then integrates into the host cell’s genome with the help of the integrase enzyme.
4. The integrated viral DNA hijacks the host cell’s machinery to produce new viral RNA, proteins, and enzymes like protease.
5. These components assemble into new virus particles that bud off from the host cell, releasing mature virions capable of infecting other cells.
6. As HIV replicates, it progressively destroys CD4+ T cells, impairing the immune system’s ability to fight infections and diseases.
7. The gradual depletion of CD4+ T cells leads to the development of Acquired Immunodeficiency Syndrome (AIDS), the most severe stage of HIV infection, characterized by opportunistic infections and cancers.