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Pathophysiology > Exam 4 part 2 > Flashcards

Exam 4 part 2 Flashcards

1
Q

Complete fracture

A

When the bone is broken entirely

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2
Q

Incomplete fracture

A

Damage to the bone, but it’s still in one piece

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3
Q

Open fracture

A

A piece of bone protrudes from the skin. Leads to infection most commonly

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4
Q

Closed fracture

A

Occurs inside the skin. Can be incomplete or complete

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5
Q

Comminuted fracture

A

Bone breaks in two or more fragments. Particularly difficult to reset.

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6
Q

Linear fracture

A

Runs parallel to long axis of bone

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7
Q

Oblique fracture

A

Occurs at an oblique angle to the long shaft of the bone

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8
Q

Spiral fracture

A

Circle bone fractures that result from twisting forces

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9
Q

Transverse fracture

A

Occurs straight across the bone

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10
Q

Greenstick fracture

A

Break in one portion of the bone with splintering of the inner bone surface.

Most commonly in children and the elderly.

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11
Q

Torus fracture

A

No break, just cracking

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12
Q

Bowing fracture

A

Longitudinal force applied that causes bending

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13
Q

Stress fractures

A

Microfractures commonly seen in athletes.

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14
Q

Transchondral fractures

A

Separation of cartilage surfaces from the main bone

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15
Q

Manifestations of fractures

A
  • Unnatural alignment
  • Swelling
  • Muscle spasm
  • Tenderness
  • Pain
  • Impaired sensation
  • Decreased mobility
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16
Q

Types of fracture healing

A
  • Direct (primary) healing

- Indirect (secondary) healing

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17
Q

Direct (primary) healing

A

—Occurs when bone cortices are in contact with one another
—Occurs with surgical fixation
—No callus formation

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18
Q

Indirect (secondary) healing

A

—Involves formation of callus
—Eventual remodeling of solid bone
—Occur when fracture treated with cast or other nonsurgical method

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19
Q

Reduction

A

realigning the broken bone fragments

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20
Q

open Reduction

A

-Realigning the bone with surgery

fragments are manipulated into alignment under direct visualization

Fixation is used to hold the broken bones in an aligned position

-Internal Fixation-screws, plates, nails or wires
ORIF- Open Reduction Internal Fixation is most common
-External Fixation- pins or rods are surgically placed into uninjured bone near the fracture site and then stabilized with external frame of bars
high risk of infection

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21
Q

Closed Reduction

A

treats the fracture without surgery (w/o opening the skin)

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22
Q

Immobilization

A

-holding the fragments in place

use a splint or cast (6-8 weeks) Used after closed reduction

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23
Q

Improper reduction or immobilization of a fractured bone may result in

A

Nonunion- failure of the bone ends to grow together
the gap between the broken ends of the bone fills with fibrocartilage instead of bone
usually occurs in people with other problems (diabetes, smoking, etc)
Delayed Union- union that occurs 8-9 months after fracture (also affected by diabetes, smoking..)
Malunion- The bone heals in the incorrect position

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24
Q

Dislocation

A
  • Displacement of one or more bones in a joint

- Opposing joint surfaces entirely lose contact

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25
Q

Subluxation

A
  • Injury which occurs when contact between opposing joint surfaces is only partially lost
    * **Can be AQUIRED, there is PAIN, @ joint-may need REDUCTION
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26
Q

Sprains

A

Ligament tear–wrist, ankle, knee most common areas

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27
Q

Strains

A

Tearing or stretching of a muscle or tendon

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28
Q

Avulsion

A

Complete separation of tendon or ligament from bony attachment site.

Young athletes, distance runners
STAGING- 1ST–3RD Degree–1st Least 3rd Complete Avulsion
**Determines therapy and treatment
**The larger the injury–the more chance to REINJURE

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29
Q

Tendinopathy

A

Painful inflammation of tendons (Tendonitis)

Most common form of Epicondylopathy

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30
Q

Epicondylopathy

A

result of Tendonitis

  • Medial : also know as the Golfers elbow. Is the result of forces affecting the forearm muscles responsible for forearm flexion and pronation
  • Lateral : also know as Tennis elbow. Is caused by irritation and overstretching of the extensor carpi radialis brevis tendon and forearm extensor muscles resulting in tissue degradation.

S &S : Localized to one side of the joint, local tenderness and more pain with active motion rather than passive movement

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31
Q

Bursitis

A

is the painful inflammation of the Bursae; Bursae are small sacs lined with synovial membrane and filled with synovial fluid that are located between bony prominences and soft tissue, such as : tendons, muscles, and ligaments
Common in the shoulder, Hips, and Elbows
It is important when diagnosing and treating Bursitis to make sure that there is no infection in the Bursa. If so…

S & S would be pain, Redness, and low grade fever

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32
Q

Rhabdomyolysis

A

Rapid breakdown of muscle that causes the release of muscle cell contents (including myoglobin) into extracellular space and bloodstream. Possibly caused by physical interruptions in the muscle (sarcolemal) membrane.

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33
Q

Patho of rhabdomyolysis

A

-Delta lesions in membrane release cellular contents.
Relatively rare, but has many causes and can cause serious complications:
-Hyperkalemia (due to release of intracellular potassium into circulation)
-Metabolic acidosis (due to release of intracellular phosphorus and sulfate)
-*Acute renal failure (because myoglobin precipitates in the renal tubules, obstructing flow and producing injury)
-Disseminated intravascular coagulation (DIC) (Sarcolemma damage starts the clotting cascade)

*Most important complication

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34
Q

Manifestations of rhabdomyolysis

A

Classic Triad of symptoms:
Muscle pain
Weakness
Dark urine/myoglobinuria

Along with the release of myoglobin, creatine kinase and other serum enzymes are released in massive quantities.
Loss of potassium/phosphate/nucleotides/creatinine/creatine

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35
Q

Compartment Syndrome

A

Compartment syndrome is increased pressure within one of the body’s compartments which contains muscles and nerves.

Compartment syndrome occurs after a traumatic injury or as a result of any condition that can increase compartment content such as a car crash, bone fracture, edema, or infarction. The trauma causes a severe high pressure in the compartment which results in insufficient blood supply to muscles and nerves.

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36
Q

Manifestations of compartment syndrome

A

The major signs and symptoms are the five P’s:

  1. Pain (out of proportion to the injury)
  2. Pallor
  3. Pulse decline
  4. Pressure Increased
  5. Paresthesia.

The weight of a limp limb could generate enough pressure to produce muscle ischemia.

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37
Q

Malignant Hyperthermia

A

It is a rare genetic disorder of the muscles. It is most common in children and adolescents. It is caused by a hyper metabolic reaction to certain anesthetics or succinylcholine (depolarizing muscle relaxants). The body reacts with an altered or prolonged release of intercellular calcium.

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38
Q

Manifestations of Malignant Hyperthermia

A
  • Hypermetabolism: Extremely high body temp
  • muscle rigidity
  • rhabdomyolysis
  • sinus tachycardia
  • respiratory acidosis
  • masseter muscle spasm/muscle contractions.
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39
Q

Osteoporosis

A

“porous bone”.

Metabolic disease. Old bone is being resorbed faster than new bone is being made. This progresses slowly until fracture (fx) occurs. A bone density test of 2.5 or more below standard is indicative of osteoporosis. Can be total skeleton or just a segment.

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40
Q

Risk factors for osteoporosis

A 
genetics    
fair, pale            
decrease in calcium intake    
caucasian    
sedentary life-style        
decrease in vitamin D intake
age        
smoking
female        
early menopause
small, thin    
increase alcohol consumption
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41
Q

Patho of osteoperosis

A 
Osteoporosis develops when remodeling cycle is disrupted.
        Bone resorption (osteoclasts) increases.
        Bone formation (osteoblasts) decreases.
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42
Q

Manifestations of osteoperosis

A

Depends on bone, pain, bone deformity -> advanced stage, Kyphosis “hunchback” ->
vertebral bone collapse.

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43
Q

Osteomalacia

A

“softening of the bone”

Normal amount of collagen but not enough calcium, bone volume is unchanged.

This is caused by a Vitamin D deficiency.

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44
Q

Manifestations of osteomalacia

A
  • pain in musculoskeletal system
  • pain particularly in hips
  • waddling gait
  • bowed legs or “knock knees”
  • **low back pain earliest complaint may start in 20’s
  • pain in ribs/feet/vertebral column
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45
Q

Paget’s disease

A

Also called “osteitis deformans”; it is a state of increased metabolic activity in the bone and is an abnormal & excessive bone remodeling (both resorption and formation)

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46
Q

Patho of Paget’s Disease

A
  • Begins with excessive breakdown of bone
  • Results in laying down of unorganized bone
  • Trabecular network diminishes (this network is the support structure of the bones)
  • Bone marrow is replaced by extremely vascular fibrous tissue
  • Formation of abnormal new bone at accelerated rate
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47
Q

Manifestations of Paget’s Disease

A

Evident in skull first (it thickens and assumes asymmetric shape)

  • deafness
  • sensory deficits
  • dementia and HA
  • all d/t increased pressure on brain created by thickened portions
  • stress fractures in lower extremities d/t decrease in trabecular network
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48
Q

Osteomyelitis

A

a bone infection most often caused by bacteria; however, fungi, parasites and viruses also can cause bone infection. It is a common complication of sickle cell anemia and low oxygen tension.

Regardless of the source of the pathogen, the pathologic features of bone infection are similar to those in any other body tissue.

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49
Q

Manifestations of osetomyelitis

A

vary with the age of the individual, the site of involvement, the initiating even, the infecting organism, and the type of infection - acute, subacute or chronic.

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50
Q

Acute osteomyelitis

A

causes abrupt onset of inflammation. If an acute infection is not completely eliminated, the disease may become subacute or chronic.

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51
Q

subacute and chronic osteomyelitis

A

subacute osteomyelitis, signs and symptoms are usually vague. In the chronic stage, infection is indolent or silent between exacerbations.

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52
Q

Exogenous Osteomyelitis

A

an infection that enters from outside the body, for example through open fractures, penetrating wounds, or surgical procedures.

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53
Q

Endogenous Osteomyelitis

A

caused by pathogens carried in the blood from sites of infection elsewhere in the body.

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54
Q

Hematogenous Osteomyelitis

A

( a common form of osteomyelitis) is usually found in infants, children and elderly persons. Microorganisms reach the vertebrae through arteries, veins, or lympathic vessels.

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55
Q

Rheumatoid Arthritis (RA)

A

· Chronic, systemic, inflammatory autoimmune disease

· Joint swelling and tenderness and destruction of synovial joints

56
Q

Patho of rheumatoid arthritis

A

Cartilage damage in RA is result of 3 processes

  1. neutrophils & other cells become activated degrading articular cartilage
  2. enzymatic breakdown of cartilage and bone
  3. synovium converted into pannus
57
Q

Manifestations of rheumatoid arthritis

A

· Onset usually insidious
· Begins with general systemic manifestations of inflammation
· Fever, fatigue, weakness, anorexia, weight loss, generalized aching and stiffness
· Local manifestations appear gradually
· Joints become painful, tender, and stiff
· Pain early in disease caused by pressure from swelling
· Late pain is caused by sclerosis of subchondral bone and new bone formation

58
Q

Osteoarthritis (OA)

A

· Common age related disorder of synovial joints
· Local areas of loss & damage of articular cartilage
· New bone formation of joint margins
· Thickening of joint capsule

59
Q

Patho of osteoarthritis

A

Primary defect is loss of articular cartilage
— Cartilage becomes thin and absent in some areas
— Unprotected bone becomes sclerotic (dense & hard)

60
Q

Manifestations of osteoarthritis

A

· Appear in 5th or 6th decade of life
· Pain in one or more joints with weight bearing, use of the joint, or load bearing
· Resting the joint relieves pain
· Stiffness in joints
· Enlargement or swelling of joints
· Tenderness
· Limited ROM
· Paresthesias (numbness, tingling)

61
Q

Ankylosing Spondylitis (AS)

A
  • Chronic inflammatory joint disease
  • It is a systemic autoimmune disease
  • Characterized by stiffening and fusion (ankylosis) of the spine and sacroiliac joints
62
Q

Patho of ankylosing spindylitis

A
  • AS begins with inflammation of fibrocartilage in cartilaginous joints
    • first affects the sacroiliac joint

Inflammatory cells infiltrate the fibrous tissue of the joint capsule, eroding bone and fibrocartilage

  • this leads to repair of the bone, over and over again, leading to ossified scar tissue
  • this then causes joints to fuse or lose flexibility
63
Q

Manifestations of ankylosing spindylitis

A
  • Low back pain and stiffness
  • Worse after prolonged rest and alleviated by physical activity
  • Early morning stiffness
64
Q

Gout

A
  • Gout is a syndrome caused by incomplete purine metabolism, resulting in excess serum uric acid levels (hyperuricemia)
  • Characterized by inflammation and pain of the joints
  • Caused by either excessive uric acid production or underexcretion of uric acid by kidneys
65
Q

Patho of gout

A
  • linked to purine metabolism and kidney function
  • Crystals of Uric acid are formed and then deposit into the joints
  • Urate excretion from the kidneys slows down
66
Q

Manifestations of gout

A
  • Primary symptom is severe pain
  • Hyperuricemia
  • recurrent abrupt attacks at a single joint (typically the big toe)
  • joint becomes hot, red, and extremely tender. Can be swollen. Usually at night.
  • deposits of tophi in and around the joints
  • renal disease
  • renal stones

50% are in big toe; other joints affected can be- heel, ankle, knee, wrist, elbow

67
Q

Fibromyalgia

A

Diffuse pain, fatigue, increased sensitivity to TOUCH

Chronic Musculoskeletal SYNDROME

68
Q

Patho of fibromyalgia

A

Genetic factors
Alterations in genes affecting serotonin, catecholamines, and dopamine
these are stress receptors and sensory processing due to stress triggers

69
Q

Manifestations of fibromyalgia

A
  • Diffuse, chronic pain
  • CONFIRMATION-TENDERNESS IN 11 OF 18 TENDER POINTS
  • Burning or gnawing pain
  • NO systemic process
  • Anxiety & Depression- Difficult to diagnose
70
Q

Osteosarcoma

A

Most common malignant bone forming tumor

71
Q

Chondrosarcoma

A

2nd most common tumor; middle aged or older and peaks in the 6th decade of life; cartilage forming tumor (chondroid cartilage) ; Giant cell tumor that can grow rapidly

72
Q

Fibrosarcoma

A

Most common Collagenic tumor producing fibrous connective tissue and can affect bone or soft tissue( collagen forming tumor) ; Most common in the Femur or Tibia

73
Q

Giant Cell Tumor

A

6th most common primary bone tumor; It is generally benign but can become malignant after radiation treatment. Wide age range but normally not below 10 years old or over 70 years old ( mostly btwn 20-40 yrs olds are diagnosed) and tend to affect Females more often than males.
It is a solitary , circumscribed tumor that causes bone resorption bcs of its osteoclastic origin - located in the center of the epiphysis in the femur, tibia, radius, or humerus.

S & S - pain, local swelling, and limitation of movement

74
Q

Rhabdomyosarcoma

A

Rare benign tumor of the muscle that generally occurs in the tongue, neck muscles, larynx, uvula, nasal cavity, axilla, vulva, or heart. highly malignant and metastasizes rapidly; common in infants, children, and teenagers and located in the muscle tissue of head, neck and genitourinary tract with remainder found in the trunk and extremities.

75
Q

Antidiuretic hormone

A

Produced in posterior pituitary.

Excess amounts of this hormone results in water retention and a hypoosmolar state, where as deficiencies in the amount or response to ADH result in serum hyperosmolarity.

76
Q

Syndrome of Inappropriate Antidiuretic Hormone Secretion

A

Characterized by high levels of ADH without normal physiologic stimuli for its release.

Caused by:

  • Ectopic production of ADH by tumors and cancers in other areas of the body
  • Surgery (causes temporary SIADH)
  • Pulmonary and CNS disorders
  • Medications
77
Q

Patho of SIADH

A

Enhanced water retention due to increase of ADH. ADH increases renal collecting duct permeability to water which increases water reabsorption by the kidneys.

Sodium in body serum is diluted, causing hyponatremia and urine that is inappropriately concentrated

78
Q

Manifestations of SIADH

A 
Manifestations of hyponatrimia:
    mild:
Thirst
Impaired taste
Anorexia
Dyspnea on exertion
Fatigue
Dulled senses
    moderate:
GI problems (vomiting/cramps)
     severe: 
Confusion
Lethargy
Muscle twitching
Convulsions
Neurologic damage
79
Q

Diabetes Insipidus

A

Characterized by insufficient activity of ADH, leading to polyuria (frequent urination) and polydipsia (frequent drinking)

Two major causes:
Neurogenic: Caused by the insufficient secretion of ADH. Occurs when any organic lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes with ADH synthesis, transport, or release.
Well recognized complication of closed head injury

Nephrogenic: Caused by inadequate response of the renal tubules to ADH, which is usually acquired or genetic. Related to damage of the tubules by drugs or disorders.

80
Q

Patho of diabetes insipidus

A

Partially or total inability to concentrate urine. Large volumes of diluted urine leading to plasma osmolarity.

As water is lost in the urine, serum hypernatremia and hyperosmolarity occur.

81
Q

Manifestations of diabetes insipidus

A
  • Polyuria/nocturia
  • Continuous thirst and polydispia
  • Long term patients will develop large bladder capacity and hydronephrosis
82
Q

Hypopituitarism

A

A condition of the anterior pituitary. It is the absence of one or more SELECTED hormone (TSH, FSH, LH, TSH, ACTH, or GH).

Some possible injuries of the pituitary include vascular infarction, aneurysm, tumor, or any other condition that would impede secretion.

83
Q

Low release levels of

TSH-Thyroid

A 
Cold Intolerance
Skin Dryness
Mild Myxedema
Lethargy
Decreased Metabolic Rate
84
Q

Low release levels of

FSH/LH-Testes and Ovaries

A

Loss of sex drive
Women: Loss of period
Atrophy of uterus

Men: testicles smaller
Less Hair

85
Q

Low release levels of

ACTH-Adrenal Cortex

A 
Loss of Cortisol-Life threatening w/I 2 weeks
Nasuea/Vomiting
Anorexia
Fatigue
Weakness
Hypoglycemia
Decreased Aldosterone secretion
Decreased urine output
86
Q

Low release levels of

GH-Entire Body

A 
Adults: Fatigue
Social Withdraw
Loss of Motivation
Osteoporosis
Altered Body Composition
Children: Dwarfism
87
Q

Hyperpituitarism

A

A condition of the anterior pituitary. It is the hypersecretion of various hormone(s) of the pituitary.
It is usually due to local invasion of a pituitary tumor (adenoma).

88
Q

Manifestations of hyperpituitarism

A

The manifestations vary according to tumor growth and the hormone that is being secreted. Most commonly we see neurological symptoms such headaches, fatigue, neck pain, stiffness, and visual changes. The pressure of the tumor could result in thyroid and adrenal hypofunction leading to symptoms of hypothyroidism and hypocortisolism.

89
Q

panhypopituitarism

A

Low levels of all the anterior pituitary hormones.

  • All hormones of the anterior pituitary gland are deficient. (TSH, corticotropins, Substance B and Prolactin).
  • cortisol deficiency from lack of ACTH, potentially life threatening.
  • thyroid deficiency from lack of TSH, rare, cold intolerance, skin dryness, mild myxedema, lethargy and decreased metabolic rate.
  • loss of secondary sex characteristics from lack of follicle-stimulating hormone FSH
90
Q

Manifestations of pituitary adenomas

A

These tumors are very small… cellular and are unique to the types of cells they originate from.

  • Hypersecretion of that hormone
  • Surrounding cell types will get pinched off and decreased

Manifestations occur due to cell changes as well as swelling.

  • Headaches
  • Fatigue
  • Stiff neck
  • Visual changes
  • Neuro changes
91
Q

Hypersecretion of growth hormone

A

Hypersecretion of growth hormone (Acromegaly) occurs d/t continuous exposure to the growth hormone (GH) and insulin like growth factor 1; also d/t GH-secreting pituitary adenoma

92
Q

Patho of hypersecretion of GH

A

In GH secreting adenomas, the usual GH baseline secretion pattern and GH sleep-related GH peaks are lost; secretion of GH is never completely suppressed; GH secretion occurs at all times of day and is unpredictable; if this happens in children whose epiphyseal plates have not yet closed, it’s called giantism (not acromegaly), where skeletal growth is excessive; if this happens in adults, it causes connective tissue proliferation and increased cytoplasmic matrix as well as bony proliferation.

93
Q

Manifestations of hypersecretion of GH

A
  • Hypertrophy of sweat and sebaceous glands
  • Course skin/hair
  • Cardiomegaly/hypertension
  • Sexual dysfunction
  • Peripheral neuropathy
  • Visual field deficits
  • Large nose , jaw, tongue
  • Enlargement bones on face, hands and feet. Lower jaw protrudes. Prominent supraorbital ridge. Barrel chest.
  • Abnormal glucose tolerance (diabetes mellitus) S & S
  • Arthritis
  • Skeletal growth is excessive
  • Renal tubules resorption of phosphate
94
Q

Hyperthyroidism

A
  • Results from an increased level of Thyroid Hormones (TH)
  • Graves disease is most common cause– 50-80% of cases
  • higher incidence in women
95
Q

Patho of hyperthyroidism

A
  • Results from type II Hypersensitivity where there is a stimulation of Thyroid autoantibodies directly against the TSH receptor
  • stimulation of these autoantibodies, called thyroid-stimulating immunoglobulins (TSIs), stimulate the TSH receptors on the thyroid gland and result in hyperplasia (Goiter)
  • This leads the thyroid to continue producing TH, leading to an increase in TH in the body and s/s of hyperthyroidism
  • TSH is also inhibited through a negative feedback to the pituitary
  • the pituitary senses too much TH in the body, so it does not produce and release TSH
96
Q

Manifestations of hyperthyroidism

A
  • *Opthalmopathy (think of EYE PROBLEMS)
  • *exopthalmos- protrusion of the eyeballs
  • Also think of INCREASED metabolic rate and increased sensitivity
  • Tachycardia, diarrhea, warm skin, hyperreflexia
  • enlarged Thyroid

just think of “eyes”

97
Q

Patho of Hypothyroidism

A

deficient production of TH by the thyroid gland

LOW TH levels with HIGH TSH
-loss of thyroid function leads to decreased production of TH and increased secretion of TSH & TRH

  • Primary thyroid malfunction- when the thyroid is dysfunctional–resulting in low TH & High TSH
  • secondary thyroid malfunction- when the pituitary, and thus secretion of TSH, is dysfunctional (rare)
98
Q

Manifestations of hypothyroidism

A

**Myxedema- nonpitting, boggy edema, especially around the eyes, hands and feet (puffy face)

DECREASE in Metabolism and energy

  • Bradycardia
  • Constipation
99
Q

Thyrotoxic Crisis (THYROID STORM)

A
  • RARE, EMERGENCY- DEATH within 48 hours when not treated
  • Occurs in patients who are undiagnosed or partially treated hyperthyroid ds

Causes:
-excessive STRESS, such as Infection, CV and pulmonary disorders, trauma, seizures, emotional distress.

MANIFESTATIONS: hyperthermia, atrial tachydysrhythmias, heart failure, agitation, nausea, vomiting, diarrhea leading to dehy, delirium/agitation

100
Q

Manifestation of thyroid storm

A
  • hyperthermia
  • atrial tachydysrhythmias
  • heart failure
  • agitation
  • nausea
  • vomiting
  • diarrhea leading to dehydration
  • delirium/agitation

****#1 Problem Cardiac #2 Problem Dehydration

101
Q

Myxedema Coma

A

a) Medical emergency
b) Decreased LOC, hypothermia w/o shivering, hypoventilation, hypotension, hypoglycemia and
lactic acidosis
c) High Risk: older patients with severe vascular disease and with moderate or untreated

hypothyroidism.
May occur after overuse of narcotics or sedatives or post acute illness.

102
Q

Manifestation of myxedema coma

A 
-        Hypothermia without shivering
·         Hypoventilation
·         Hypotension
·         Hypoglycemia
·         Lactic Acidosis
103
Q

Hyperparathyroidism

A

Greater than normal secretion of parathyroid hormone (PTH) and hypercalcemia.

Classified as either primary or secondary.

Causes:

  • Parathyroid adenomas (most common)
  • Parathyroid hyperplasia
  • Parathyroid carcinoma
  • Genetic causes
104
Q

Patho of primary hyperparathyroidism

A

Primary: Characterized by inappropriate excess secretion of PTH by one or more of the parathyroid glands. PTH secretion is increased and is not under usual feedback control mechanisms.

Calcium level in the blood increases because of increased bone resorption and GI absorption of calcium.

105
Q

Patho of secondary hyperparathyroid hormone

A

Secondary: Response of the parathyroid glands to chronic hypocalcemia, which can be associated with decreased renal activation of Vit D.

Secretion of PTH is elevated, but it can’t achieve normal calcium levels due to deficiency of vitamin D.

106
Q

Manifestations of hyperparathyroid hormone

A
  • Hypercalcemia/hypophosphatemia Hallmark
  • Pathological facial muscular problems
  • Headache
  • Nausea and vomiting
  • Fatigue
  • Depression
  • Anorexia
  • Kidney stones
107
Q

Hypoparathyroidism

A

Abnormally low PTH levels.

Causes:

  • Damage to the parathyroid glands during thyroid surgery (most common)
  • Genetic syndromes
  • Hypomagnesemia
  • Autoimmune
108
Q

Patho of hypoparathyroidism

A

Lack of circulating PTH causes depressed serum calcium levels and increased serum phosphate levels.

In the absence of PTH, resorption of calcium from bone and regulation of calcium reabsorption from the renal tubules are impaired.

109
Q

Manifestations of hypoparathyroidism

A 
-Hypocalcemia/hyperphosphatemia **Hallmark**
Manifestations due to low calcium levels in blood:
Dry skin
Hair loss
Hypoplasia of developing teeth
Horizontal ridges on nail
Cataracts
Bone deformities
Basal ganglia calcification 
Low threshold of nerve excitement:
Tetany: muscle spasms
Hyperreflexia
Clonic-tonic seizure
Laryngeal spasms
\+Chovstek and +Trosseau signs
110
Q

Normal glucose metabolism

A

The stomach converts food/carbs into glucose, the glucose then enters the bloodstream. The pancreas normally releases insulin in response. The insulin and the glucose can then enter the cells together. In a fast or when you skip a meal, your liver pumps out glucose to meet the needs of your cells and body.

111
Q

Patho of Diabetes Mellitus- Type 1

A

Insulin dependant

In Type 1, the cells that produce the insulin (Beta Cells) were damaged or destroyed by a T-Cell autoimmune disease. The cause varies but there are several contributing factors including genetics, viruses, drugs, and or illness. The Beta Cells were damaged so the pancreas makes little to no insulin. What is produced enters the bloodstream but it’s not enough. The glucose cannot enter the cells without the insulin therefore it builds up in the blood stream.

112
Q

Patho of Diabetes Mellitus-Type 2

A

Insulin resistant

In type 2, the Beta Cells are fine therefore sufficient amounts of insulin are being produced. The defect is with the cellular receptor; the cell does not recognize the insulin and therefore does not let the insulin or glucose in. It is insulin resistant. Therefore you still end up with low intracellular glucose. In response, the pancreas thinks the cells are starving and compensates but continually pumping out insulin and eventually fails due to overproduction. Once again, we have a backup of glucose and now insulin in the bloodstream.

113
Q

Risk factors to type 1 DM

A

Autoimmune: Genetic or environmental factors. Whites have 1.5-2 times higher risk than non-whites.

114
Q

Risk factors to type 2 DM

A

Obesity, high fat and cholesterol levels, high blood pressure, smoking, sedentary lifestyle, over 30 years of age, race (highest risk for black and native Americans)

115
Q

Manifestations to type 1 DM

A

3 P’s:
Polydipsia: Increased Thirst related to intracellular dehydration.
Polyuria: Increased Urination due to hyperglycemia
Polyphagia: Increased Hunger due to cellular starvation

  • Prolonged wound healing due to impaired blood supply
  • Visual Changes/Blurry Vision due to elevated blood glucose levels
  • Cardiovascular Symptoms: Chest Pain due to diabetes contribution to formation of atherosclerosis affecting circulation.
  • Paresthesisas: Numb or tingling hands/feet
  • Weight Loss due to fluid loss and loss of tissue as fat and proteins are used for energy
  • Fatigue due to poor use of food products
  • Recurrent Infections-Yeast loves sugar
  • Rapid Onset
  • Genital Pruritus due to fungal growth
116
Q

Manifestations to type 2 DM

A 
Nonspecific:
Polydipsia: Increased Thirst
Polyuria: Increased Urination
Recurrent Infection-Yeast loves sugar
Pruritus: Itching
Visual Changes/Blurry Vision
Neuropathy Symptoms
Paresthesisas: Numb or tingling hands/feet
117
Q

Acute complications of DM

A
  • Hypoglycemia
  • Ketoacidosis (DKA)
  • Hyperosmolar hyperglycemic non-ketotic syndrome (HHNKS)
  • Somogyi effect
  • Dawn Phenomenon
118
Q

Hypoglycemia

A

(<70) (extra insulin from not eating when taking insulin meds) S/S: pallor, tremor,
anxiety, tachycardia, palpitations, hunger, poor judgement, seizure/coma, DRUNK ACTING.

119
Q

Ketoacidosis

A

(DKA) more common in Type I. S/S: metabolic acidosis, postural dizziness, CNS
depression, anorexia, nausea, abdominal pain,thirst, polyuria.

Main manifestations:
ketonuria
Kussmall respirations
Fruity acetone smelling breath.

120
Q

Hyperosmolar hyperglycemic non-ketotic syndrome (HHNKS)

A 
More common in Type II,
elderly. Fluid deficit is more profound, usually caused by dehydration. 
    Main manifestations:
really high glucose levels (>600)
small/absent amount of ketones in urine.
121
Q

Somogyi effect

A

overnight hypoglycemia, with rebound morning hyperglycemia.

122
Q

Dawn Phenomenon

A

early morning hyperglycemia with no low hypo at night.

123
Q

Chronic complications of DM

A
  • microvascular disease (retinopathies nephropathies and neuropathies)
  • macrovascular disease (coronary artery, peripheral vascular, and cerebral vascular)
124
Q

Cushing Syndrome

A

occurs when pts have been exposed to excess cortisol for long periods of time (such as when taking steroids for asthma or arthritis)

Patho: no patho is in PP or in book really; it seems lumped together with Cushing Disease

125
Q

Manifestations of Cushing syndrome AND Cushing disease

A
  • thinning of scalp hair
  • acne
  • facial flush
  • increased body and facial hair
  • moon face
  • supraclavicular fat pad
  • purple striae
  • hyperpigmentation
  • pendulous abdomen
  • trunk obesity
  • easy bruising
  • thin extremities
126
Q

Cushing disease

A

occurs from overproduction of pituitary ACTH by a pituitary adenoma or by an ectopic secreting nonpituitary tumor

ACTH-dependent/ACTH-independent hypercortisolism

127
Q

ACTH-dependent hypercortisolism

A

results from overproduction of pituitary ACTH by a pituitary adenoma or by ectopic secreting nonpituitary tumor

In ACTH- dependent hypercortisolism, the excess ACTH stimulates excess production of cortisol and there is loss of feedback control of ACTH secretion; secretion of both cortisol and adrenal androgens is increased, and cortisol-releasing hormone is inhibited

128
Q

ACTH-independent hypercortisolism

A

caused by cortisol secretion from a rare benign or malignant tumor of one or both adrenal glands

In ACTH-independent hypercortisolism, the tumors of the adrenal cortex generally only secrete cortisol and tumors secretion of cortisol exceeds normal levels, hypercortisolism occurs

129
Q

Patho of Cushing disease

A

whatever the cause, two observations consistently apply to individuals with hypercortisolism, (1) the normal diurnal or circadian secretion patterns of ACTH and cortisol are lost, and (2) there is no increase in ACTH and cortisol secretion in response to stressor.

130
Q

Hyperaldosteronism

A

Excessive secretion aldosterone by adrenal medulla.

Primary: normally from adrenal adenoma (33% of pts. with resistant hypertension)
Secondary : by secondary cause such as extra-adrenal stimuli of aldosterone secretion most often angiotensin II through a renin-dependent mechanism. (decreased circulating blood volume

131
Q

Patho of hyperaldosteronism

A

Hyperaldosteronism promotes increased renal sodium and water reabsorption with corresponding hypervolemia and hypertension and renal excretion of potassium

132
Q

Manifestations of hyperaldosteronism

A
  • Hypertension
  • increased renal sodium and water reabsorption with corresponding hypervolemia
  • Extracellular fluid overload

Edema normally does not occur with primary. -Hypokalemia and hypertension are hallmarks of primary.

133
Q

hypocortical functioning (Addison disease)

A

Hypocortisolism = Addison Disease
Hypocortisolism- low levels of cortisol secretion due to (either/or):
- inadequate stimulation of the adrenal glands by ACT
-primary inability of the adrenals to produce and secrete cortisol (and other adrenocortical hormones)

134
Q

Patho of Addison disease

A

Addison Disease is a primary adrenal insufficiency. There is an indadequate synthesis of corticosteroids and mineralocorticoids, with elevated levels of ACTH. It is caused by autoimmune mechanisms that destroys adrenal cortical cells.

135
Q

Manifestation of Addison disease

A
  • *HYPOTENSION- this is the greatest concern because it can lead to shock.
  • weakness
  • easy fatigability
  • Hyperpigmentation
  • vitilgo (loss of pigmentation)
  • Anorexia
  • Nausea & Vomiting
  • Diarrhea
136
Q

pheochromocytomas

A

Tumor on adrenal gland

Patho: sympathetic paraganliomas of the adrenal medula which secrete catecholamines on a continual
basis. 10% may be MALIGNANT
PRONE TO RUPTURE-NEEDS TO BE REMOVED OR CAN BLEED OUT

137
Q

Manifestations of pheochromocytomas

A 
Hypertension
Headache
pallor
diaphoresis
tachycardia
palpitations
glucose intolerance

Pathophysiology (6 decks)

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