Real World Flashcards

1
Q

What do topical calcineurin inhibitors do? (ex. Elidel - aka pimecrolimus)

A

There are two types of topical calcineurin inhibitors called tacrolimus ointment (Protopic 0.03% and 0.1%) and pimecrolimus cream (Elidel). They are classified as immunomodulating agents. This means that they act on the immune system to reduce skin inflammation. Both tacrolimus and pimecrolimus block a chemical called calcineurin which activates inflammation in the skin and causes redness and itching of the skin.
Tacrolimus ointment and pimecrolimus cream are licensed in the UK for the treatment of atopic eczema (atopic dermatitis) in adults, and children over the age of 2 years. Tacrolimus comes in two strengths; 0.03% (weaker) and 0.1% (stronger); the weaker preparation is licensed to be used in children between the ages of 2 and 16, and the stronger preparation in adults over the age of 16. Tacrolimus ointment is also licensed for the prevention of flares of atopic eczema in adults. These topical treatments can also be prescribed for a number of other inflammatory skin conditions such as psoriasis (particularly on the face), seborrhoeic eczema (seborrhoeic dermatitis), lichen planus, lichen sclerosus, vitiligo, cutaneous lupus erythematosus and pityriasis alba but the calcineurin inhibitors are not officially licensed for these skin conditions.

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2
Q

What is psychogenic syndrome

A

An external stimuli shocks someone so severly the brain suffers an electric short. Can have the presentation of seizure or coma.
Definitive test: raise the patients arm above hus face and let go. A patient in a psychogenic coma has enough capacity to avoid hitting himself.
The treatment: speak reassuringly until your words connect and the patients awaken

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3
Q

Juvenile rheumatoid arthritis (JRA), often referred to by doctors today as juvenile idiopathic arthritis (JIA)

A

is a type of arthritis that causes joint inflammation and stiffness for more than six weeks in a child aged 16 or younger. It affects approximately 50,000 children in the United States

Juvenile Arthritis Progression:

Over time, children with oligoarthritis (arthritis that affects four or fewer joints) tend to outgrow arthritis, Ilowite says. But for some, the arthritis can go on to affect more joints.

Polyarthritis (arthritis affecting five or more joints), on the other hand, continues to be active and can cause irreversible damage if not treated, he says.

And for children with systemic arthritis, about 40 percent will find that their arthritis goes away after a year or two, while 35 percent will have it for several years, Ilowite says. “About 25 percent have severe unrelenting arthritis that can be destructive,” he says.

Psoriatic arthritis (a type of arthritis associated with the skin condition psoriasis) is more variable. “It can be in a few joints, it can be in a lot of joints, it can be persistent, it can go away, or it can fluctuate,” he says.

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4
Q

Ciclopirox (the shampoo)

A

is a synthetic antifungal agent for topical dermatologic treatment of superficial mycoses. It is most useful against Tinea versicolor. It is sold under many brand names worldwide
Ciclopirox is indicated for the treatment of tinea pedis and tinea corporis due to Trichophyton rubrum, Trichophyton mentagrophytes and Epidermophyton floccosum, as well as seborrheic dermatitis.
In contrast to the azoles and other antimycotic drugs, the mechanism of action of ciclopirox is poorly understood.
However, loss of function of certain catalase and peroxidase enzymes has been implicated as the mechanism of action, as well as various other components of cellular metabolism

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5
Q

What is C-reactive protein?

A

A pentameric protein released by the liver in response to inflammation and amplify it. CRP levels rise dramatically in the first 6-10 hours of an infection or injury. The levels can reach 500x baseline level of CRP. Once CRP is in the bloodstream, it enters tissues that are not infected/injured and alerts them of impending attack. IN response to CRP, tissues will produce mediators of inflammation that further promote the inflammation, cytokines.

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6
Q

What is C-peptide?

A

C-peptide is a product that is created when the hormone insulin is produced and released into the body. The insulin C-peptide test measures the amount of this product in the blood.

C-peptide is measured to tell the difference between insulin the body produces and insulin someone injects into their body.

Someone with type 1 or type 2 diabetes may have their C-peptide level measured to see if their body is still producing any insulin. It may also be measured in cases of low blood sugar to see if the person’s body is producing too much insulin.

C-peptide level is based on blood sugar level. C-peptide is a sign that your body is producing insulin. A low level (or no C-peptide) indicates that your pancreas is producing little or no insulin.

A low level may be normal if you have not eaten recently. Your blood sugar and insulin levels would naturally be low then.
A low level is abnormal if your blood sugar is high and your body should be making insulin at that time.

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7
Q

Lorazepam

lady in what the health takes it for stress

A

Lorazepam belongs to a group of drugs called benzodiazepines. It affects chemicals in the brain that may be unbalanced in people with anxiety.

Lorazepam is used to treat anxiety disorders.
It can treat seizure disorders, such as epilepsy. It can also be used before surgery and medical procedures to relieve anxiety.

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8
Q

What are the Z-drugs?

A

Three distinct groups of CNS sedative-hypnotics:

  • Zolpidem (Stilnoct, Ambien, Ambien CR, Intermezzo, Stilnox) - 1.5-2.4 hr half life
  • Zopiclone (Imovane, Zimovane, Imrest), eszopiclone (Lunesta) - 1.4 – 4.5 hours
  • *Zaleplon (Sonata, Starnoc, Andante): 1 hr half life

they work in a similar way to the benzodiazepine drugs inside the brain. They are GABA agonists meaning they somewhat mimic the action of gamma-Aminobutyric acid, the inhibitory neurotransmitter and thereby induce sleepiness. Benzodiazepines act on GABA-A receptors that include subunits of the alpha-1, alpha-2, alpha-3, and other classes. The Z-drugs are more selective for the alpha-1 subclass which seems to drive sleepiness but not anti-anxiety.

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9
Q

Cyclobenzaprine

A

Cyclobenzaprine, sold under the brand name Flexeril among others, is a muscle relaxer medication used to relieve skeletal muscle spasms and associated pain in acute musculoskeletal conditions.[5] It is the best-studied drug for this application.[6] It has also been used off-label for fibromyalgia treatment.[7]

After sustaining an injury, painful muscle spasms may occur to stabilize the affected body part and prevent further damage. Cyclobenzaprine is used to treat such muscle spasms associated with acute, painful musculoskeletal conditions.[5] It decreases pain in the first two weeks,[6][9] peaking in the first few days, but has no proven benefit after two weeks.[6][10] Since no benefit is proven beyond that, therapy should not be continued long-term.[11] It is not useful for spasticity due to neurologic conditions such as cerebral palsy

Side effects: significantly increased rates of drowsiness (38% of patients), dry mouth (24%), dizziness (10%), and adverse events of any kind in patients taking cyclobenzaprine versus placebo

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10
Q

Topirmate (brand name topamax)

A

Topiramate (brand name Topamax) is an anticonvulsant (antiepilepsy) drug. In late 2012, topiramate was approved by the United States Food and Drug Administration (FDA) in combination with phentermine for weight loss. The drug had previously been used off-label for this purpose.
Topiramate is used to treat epilepsy in children and adults, and it was originally used as an anticonvulsant.[7] In children, it is indicated for the treatment of Lennox-Gastaut syndrome, a disorder that causes seizures and developmental delay. It is also Food and Drug Administration (FDA) approved for, and most frequently prescribed for, the prevention of migraines.[7] The drug is also used to treat migraines due to the effect it has on the blood vessels in the brain. It has been found to be increasingly effective for migraine sufferers with limited side effects.

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11
Q

Prozac: Fluoxetine

A

Selective Serotonin Reuptake Inhibitor (SSRI)

It can treat depression, obsessive-compulsive disorder (OCD), bulimia nervosa, and panic disorder.

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12
Q

What does a Cpap machine do?

A

Continuous positive airway pressure therapy (CPAP ) uses a machine to help a person who has obstructive sleep apnea (OSA) breathe more easily during sleep. A CPAP machine increases air pressure in your throat so that your airway doesn’t collapse when you breathe in.
It does this by gently blowing air when you inhale to increase pressure on the walls. When you exhale, there is still continuous air being blown to keep the airway open. The blown air pushes the carbon dioxide out through tiny holes in the mask

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13
Q

What is osteoarthritis?

A

Degeneration of joint cartilage and the underlying bone, most common from 65 onward. It causes pain and stiffness, especially in the hip, knee, lower back, neck, big toe, small joints of fingers and thumb joints. The most common chronic condition of the joints, affecting 27 million Americans.

MOA: cartilage breaks down causing pain, swelling and problems moving the joint. As OA worsens over time, bones may break down and develop growths caused spurs. Bits of bone and cartilage can chip off, an inflammatory process occurs and cytokines and enzymes develop that further damage the cartilage.

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14
Q

Does calcium lower increase bone health?

A

“calcium, vitamin D, milk consumption, and hip fractures: a prospective study among postmenopausal women” - conclusion: an adequate vitamin D intake in associated with a lower risk of osteoporotic hip fractures in postmenopausal women. Neither milk nor a high-calcium diet appears to reduce risk. Because women commonly consume less than the recommended intake of vitamin D, supplement use or dark fish consumption may be prudent

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15
Q

What are casomorphins?

A

Casomorphins are peptides derived from the digestion of milk protein casein which is what makes up dairy products. They go to brain and attach to the same receptor that heroin attaches to. They are not as strong as heroin, the cheese brings you back. Can play a role in SCIDs, fetal sudden death syndrome, that is why babies are recommended to drink maternal milk

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16
Q

How does diabetes cause kidney disease.

A

When our bodies digest the protein we eat, the process creates waste products. In the kidneys, millions of tiny blood vessels (capillaries) with even tinier holes in them act as filters. As blood flows through the blood vessels, small molecules such as waste products squeeze through the holes. These waste products become part of the urine. Useful substances, such as protein and red blood cells, are too big to pass through the holes in the filter and stay in the blood.

Diabetes can damage this system. High levels of blood glucose make the kidneys filter too much blood. All this extra work is hard on the filters. After many years, they start to leak and useful protein is lost in the urine. Having small amounts of protein in the urine is called microalbuminuria.

When kidney disease is diagnosed early, during microalbuminuria, several treatments may keep kidney disease from getting worse. Having larger amounts of protein in the urine is called macroalbuminuria. When kidney disease is caught later during macroalbuminuria, end-stage renal disease, or ESRD, usually follows.

In time, the stress of overwork causes the kidneys to lose their filtering ability. Waste products then start to build up in the blood. Finally, the kidneys fail. This failure, ESRD, is very serious. A person with ESRD needs to have a kidney transplant or to have the blood filtered by machine (dialysis).

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17
Q

What is protamine?

A

Heparin is often given as an emergency anticoagulant. Heparin is a proteoglycan with a ton of negative charges but the danger is bleeding out. The antidote is PROTamine which has a ton of positive charges to counter heparin.

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18
Q

What is melanoma?

A

Melanoma, also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes.[1] Melanomas typically occur in the skin but may rarely occur in the mouth, intestines, or eye.[1][2] In women they most commonly occur on the legs, while in men they are most common on the back. Sometimes they develop from a mole with concerning changes including an increase in size, irregular edges, change in color, itchiness, or skin breakdown.

The primary cause of melanoma is ultraviolet light (UV) exposure in those with low levels of skin pigment.[2][7] The UV light may be from either the sun or from other sources, such as tanning devices. About 25% develop from moles.[2] Those with many moles, a history of affected family members, and who have poor immune function are at greater risk.[1] A number of rare genetic defects such as xeroderma pigmentosum also increase risk.[8] Diagnosis is by biopsy of any concerning skin lesion.

Melanoma is the most dangerous type of skin cancer. Globally, in 2012, it newly occurred in 232,000 people.[2] In 2015 there were 3.1 million with active disease which resulted in 59,800 deaths.[5][6] Australia and New Zealand have the highest rates of melanoma in the world. There are also high rates in Northern Europe and North America, while it is less common in Asia, Africa, and Latin America.[2] Melanoma is more common in men than women.[8] Melanoma has become more common since the 1960s in areas that are mostly Caucasian.[2][8]

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19
Q

Xeroderma pigmentosum

A

Xeroderma pigmentosum (XP) is a rare autosomal recessive genetic disorder of DNA repair in which the ability to repair damage caused by ultraviolet (UV) light is deficient.[2 In extreme cases, all exposure to sunlight must be forbidden, no matter how small; as such, individuals with the disease are often colloquially referred to as “Moon child”.[3] Multiple basal cell carcinomas (basaliomas) and other skin malignancies frequently occur at a young age in those with XP; metastatic malignant melanoma and squamous cell carcinoma[4] are the two most common causes of death in XP victims. This disease is present in both genders and in all races, with an incidence of 1:250,000 in the United States.[5] XP is roughly six times more common in Japanese people[4] than in other groups.

Symptoms include:

Severe sunburn when exposed to only small amounts of sunlight. These often occur during a child’s first exposure to sunlight.
Development of many freckles at an early age
Rough-surfaced growths (solar keratoses), and skin cancers
Eyes that are painfully sensitive to the sun and may easily become irritated, bloodshot and clouded
Blistering or freckling on minimum sun exposure
Spider Veins
Limited growth of hair on chest and legs
Scaly skin
Dry skin
Irregular dark spots on the skin
Corneal ulcerations

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20
Q

Describe isoniazid

A

Isoniazid, also known as isonicotinylhydrazide (INH), is an antibiotic used for the treatment of tuberculosis.[1] For active tuberculosis it is often used together with rifampicin, pyrazinamide, and either streptomycin or ethambutol.[2] For latent tuberculosis it is often used by itself. It may also be used for atypical types of mycobacteria, such as M. avium, M. kansasii, and M. xenopi. It is usually taken by mouth but may be used by injection into muscle.

Common side effect include increased blood levels of liver enzymes and numbness in the hands and feet. Serious side effects may include liver inflammation.[1] It is unclear if use during pregnancy is safe for the baby. Use during breastfeeding is likely okay.[3] Pyridoxine (B6) may be given to reduce the risk of side effects.[4] Isoniazid works in part by disrupting the formation of the bacteria’s cell wall which results in cell death.[1]

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21
Q

What is lidocaine?

A

anesthetic and anti-arrhythmic agent

Lidocaine is a medication used to numb tissue in a specific area.[4] It is also used to treat ventricular tachycardia and to perform nerve blocks. Lidocaine mixed with a small amount of adrenaline (epinephrine) is available to allow larger doses for numbing, to decrease bleeding, and to make the numbing effect last longer.[4] When used as an injectable, it typically begins working within four minutes and lasts for half an hour to three hours.[4][5] Lidocaine mixtures may also be applied directly to the skin or mucous membranes to numb the area

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22
Q

What is atropine used for with the heart?

A

Injections of atropine are used in the treatment of bradycardia (a heart rate < 60 beats per minute).

Atropine was previously included in international resuscitation guidelines for use in cardiac arrest associated with asystole and PEA, but was removed from these guidelines in 2010 due to a lack of evidence for its effectiveness.[14] For symptomatic bradycardia, the usual dosage is 0.5 to 1 mg IV push, may repeat every 3 to 5 minutes up to a total dose of 3 mg (maximum 0.04 mg/kg).[15]

Atropine is also useful in treating second-degree heart block Mobitz type 1 (Wenckebach block), and also third-degree heart block with a high purkinje or AV-nodal escape rhythm. It is usually not effective in second-degree heart block Mobitz type 2, and in third-degree heart block with a low Purkinje or ventricular escape rhythm.

Atropine has also been used in an effort to prevent a low heart rate during intubation of children; however, evidence does not support this use.[16]

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23
Q

Metformin is the go to prescribed drug for type 2 diabetes. What does it do?

A

Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.

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24
Q

What is portacaval shunting?

A

Portacaval shunting is major surgery. It involves a large cut (incision) in the belly area (abdomen). The surgeon then makes a connection between the portal vein (which supplies most of the liver’s blood) and the inferior vena cava (the vein that drains blood from most of the lower part of the body.)

The new connection diverts blood flow away from the liver. This reduces blood pressure in the portal vein and decreases the risk for a tear (rupture) and bleeding from the veins in the esophagus and stomach.

Normally, blood coming from your esophagus, stomach, and intestines first flows through the liver. When your liver is very damaged and there are blockages, blood cannot flow through it easily. This is called portal hypertension (increased pressure and backup of the portal vein.) The veins can then break open (rupture), causing serious bleeding.

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25
Q

What is the function of the thyroid hormone

A

The thyroid keeps your metabolism under control through the action of thyroid hormone, which it makes by extracting iodine from the blood and incorporating it into thyroid hormones. Thyroid cells are unique in that they are highly specialized to absorb and use iodine. Every other cell depends on the thyroid to manage its metabolism.

The pituitary gland and hypothalamus both control the thyroid. When thyroid hormone levels drop too low, the hypothalamus secretes TSH Releasing Hormone (TRH), which alerts the pituitary to produce thyroid stimulating hormone (TSH). The thyroid responds to this chain of events by producing more hormones.

To a lesser extent, the thyroid also produces calcitonin, which helps control blood calcium levels.

26
Q

Ketosis vs; Ketoacidosis

A

Ketosis is a state the body may find itself in either as a result of raised blood glucose levels or as a part of low carb dieting.

Low levels of ketosis is perfectly normal.

However, high levels of ketosis in the short term can be serious and the long term effects of regular moderate ketosis are only partially known at the moment.

Ketosis is a state the body goes into if it needs to break down body fat for energy. The state is marked by raised levels of ketones in the blood which can be used by the body as fuel.
Ketones which are not used for fuel are excreted out of the body via the kidneys and the urine.

There is often confusion as to the difference between ketosis and ketoacidosis.

Ketosis is the state whereby the body is producing ketones. In ketosis, the level of ketones in the blood can be anything between normal to very high.

Diabetic ketoacidosis, also known as DKA, only describes the state in which the level of ketones is either high or very high. In ketoacidosis, the amount of ketones in the blood is sufficient to turn the blood acidic, which is a dangerous medical state.

When does ketosis occur?

Ketosis will take place when the body needs energy and there is not sufficient glucose available for the body.

This can typically happen when the body is lacking insulin and blood glucose levels become high.

Other causes can be the result of being on a low carb diet.

A low level of carbohydrate will lead to low levels of insulin, and therefore the body will produce ketones which do not rely on insulin to get into and fuel the body’s cells.

A further cause of ketosis, less relevant to people with diabetes, is a result of excessive alcohol consumption.

DKA is common in type 1 diabetes as this form of diabetes is associated with an absolute lack of insulin production by the islets of Langerhans. In type 2 diabetes, insulin production is present but is insufficient to meet the body’s requirements as a result of end-organ insulin resistance. Usually, these amounts of insulin are sufficient to suppress ketogenesis. If DKA occurs in someone with type 2 diabetes, their condition is called “ketosis-prone type 2 diabetes”

Consequences of DKA - cerebral edema (most dangerous complication)
Symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels)
In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as “Kussmaul respiration”).The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness).

Mechanism

The lack of insulin and corresponding elevation of glucagon leads to increased release of glucose by the liver (a process that is normally suppressed by insulin) from glycogen via glycogenolysis and also through gluconeogenesis. High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis.[3] This leads to polyuria, dehydration, and polydipsia. The absence of insulin also leads to the release of free fatty acids from adipose tissue (lipolysis), which are converted through a process called beta oxidation, again in the liver, into ketone bodies (acetoacetate and β-hydroxybutyrate). β-Hydroxybutyrate can serve as an energy source in the absence of insulin-mediated glucose delivery, and is a protective mechanism in case of starvation. The ketone bodies, however, have a low pKa and therefore turn the blood acidic (metabolic acidosis). The body initially buffers the change with the bicarbonate buffering system, but this system is quickly overwhelmed and other mechanisms must work to compensate for the acidosis.[3] One such mechanism is hyperventilation to lower the blood carbon dioxide levels (a form of compensatory respiratory alkalosis). This hyperventilation, in its extreme form, may be observed as Kussmaul respiration.[8]

Cerebral edema: Likely factors in the development of cerebral edema are dehydration, acidosis and low carbon dioxide levels; in addition, the increased level of inflammation and coagulation may, together with these factors, lead to decreased blood flow to parts of the brain, which then swells up once fluid replacement has been commenced.[10] The swelling of brain tissue leads to raised intracranial pressure ultimately leading to deat

27
Q

Prader-Willi and Angelman Syndrome genetics

A

Both are due to identical deletion on chromosome 15q and demonstrate imprinting.

Same mutation results in different phenotypes depending on whether the mutated chromosome was of maternal or paternal origin.

Prader-Willi - deletion on paternal chromosome
-mental retardation, hypogonadism, hypotonia, obesity leading to diabetes (all important markers)
Angelman - deletion on maternal chromosome
-happy puppet, with ataxic gait and inappropriate laughter, won’t be any hypogonadism, won’t be diabetes, will have mental retardation + seizures

No treatment and lifelong supervision.

28
Q

What is the difference between Cushing’s syndrome and disease

A

Cushing’s disease is a specific type of Cushing’s syndrome caused by a pituitary tumor leading to excessive production of ACTH (adrenocorticotropic hormone). Excessive ACTH stimulates the adrenal cortex to produce high levels of cortisol, producing the disease state.

29
Q

What are characteristic symptoms of HIV

A
  • CD4+T cell count below 500
  • chills
  • fever
  • oral thrush
  • generalized malaise
  • unexplained weight loss
  • dehydration
  • abdominal cramps
  • diarrhea and stool tested positive for Giardia Lamblia antigen
30
Q

Why don’t you use beta blockers for diabetics

A

Because you will mask the symptoms of a hypoglycemic event (tachycardia)

31
Q

What is the ESR (erythrocyte sedimentation rate) FA

A

Products of inlammation (eg, fibrinogen) coat RBCs and cause aggregation. The denser RBC aggregates fall at a faster rate within a pipette tube. Often co-tested with CRP levels.
(increased ESR)
Most anemias
Infections
Inflammation (eg, giant cell [temporal] arteritis,
polymyalgia rheumatica)
Cancer (eg, metastases, multiple myeloma)
Renal disease (end-stage or nephrotic syndrome)
Pregnancy

{decreased ESR}
sickle cell anemia (altered shape)
polycythemia (increased RBCs dilute aggregation factors) 
HF
Microcytosis 
Hypofibrinogenemia 

The ESR is governed by the balance between pro-sedimentation factors, mainly fibrinogen, and those factors resisting sedimentation, namely the negative charge of the erythrocytes (zeta potential). When an inflammatory process is present, the high proportion of fibrinogen in the blood causes red blood cells to stick to each other. The red cells form stacks called ‘rouleaux,’ which settle faster, due to their increased density

32
Q

Why do anticholinergics lead to urinary retention

A

2nd order sympathetics use norepinephrine which relaxes the urinary bladder, allowing it to fill.

2nd order sacral parasympathetics use acetylcholine which stimulates the urinary bladder to contract.

Anticholinergic agents will prevent the contraction of the bladder leading to urinary retention.

33
Q

47 yr old presents with intense pain on his face arising from stimulation at the corner of his mouth. The diagnosis is trigeminal neuralgia (tic douloureux). MRI shows a vessel impinging on the root of the trigeminal nerve. Aberrant branches of what vessel would be most likely involved

A

Superior cerebellar artery, root of CNV is right under it.

34
Q

IN addition to affecting the vestibulocochlear nerve, what else would a schwannoma affect?

A

Facial nerve

Facial nerve, CN8 and labrinthine artery (branch of AICA) are all located in the internal acoustic meatus. You will see sensory loss on the face 30% of the time, while facial weakness may be seen in about 10% of cases.

35
Q

What are normal blood
glucose levels

Pre-prandial
Post-prandial

A

Preprandial - 70-99 mg/dl

Postprandial - <140 mg/dl

36
Q

What is the vascular pathology that is leading to complications in diabetes?

A

type 2 DM causes amplification of the atherosclerotic process, endothelial cell dysfunction, glycosylation of extracellular matrix proteins, and vascular denervation.

Endothelial dysfunction is a systemic pathological condition which can be broadly defined as an imbalance between vasodilating and vasoconstricting substances produced by the endothelium or overall functions of the endothelium. Normal functions of endothelial cells include production of nitric oxide (NO), regulation of platelet adhesion, coagulation, immune function, control of volume, and electrolyte content of the intravascular and extravascular spaces. Endothelial dysfunction is primarily due to reduction in NO bioavailabilty, and a marker for vascular health.

Specifically, endothelial dysfunction is associated with reduced nitric oxide production, anticoagulant properties, increased platelet aggregation, increased expression of adhesion molecules, increased expression of chemokines and cytokines, and increased reactive oxygen species production from the endothelium [10]. These all play important roles in the development of diabetic vascular complications including atherosclerosis and other vascular pathologies.

37
Q

What is diabetic wound healing?

A

Wound healing occurs as a cellular response to injury and involves activation of keratinocytes, fibroblasts, endothelial cells, macrophages, and platelets. These cell types coordinate and maintain healing through the release of many growth factors and cytokines. Defective immune cell responses or impaired recruitment within the wound site results in defective healing in diabetes. Prolonged diabetes leads to impaired wound healing, a result of defective angiogenesis.
Foot wounds followed by ulceration are a leading cause of hospital admissions for people with diabetes throughout the world and is a major comorbidity associated with diabetes, leading to extreme pain and suffering and poor quality of life for patients. Data have shown that diabetic foot ulcers (DFUs) are estimated to occur in 15% of all patients with diabetes and precede 84% of all diabetes-related lower-leg amputations.
Firstly, diabetic individuals often are unable to combat infection due to defective immune responses. Thus, even small scrapes can transition to open, infected sores. Secondly, nerve damage in diabetic patients’ results in lack of peripheral sensory function. Nerve damage may be prominent in diabetic patients resulting in a diminished capacity to notice cuts, blisters, or ulcers. Thirdly, diabetic individuals typically have diffuse atherosclerotic vessel disease that diminishes blood perfusion leading to a disruption in wound oxygenation and healing. Lastly, the DFU may also become a portal for systemic infection leading to bacteremia, septicemia, and may result in limb amputation. Importantly, delayed healing of diabetic wounds is also characterized by impaired angiogenesis and vasculogenesis responses. A series of multiple mechanisms, including decreased cell and growth factor response, lead to diminished peripheral blood flow and decreased endothelial cell proliferation and contribute to the lack of wound healing in diabetes. Excessive ROS production in diabetic patients is a primary factor contributing to wound healing deficiencies, which can be reversed using ROS antagonists

38
Q

What is likely resulting in insulin resistance.

A

High levels of lipids in the bloodstream have the potential to result in accumulation of triglycerides and their derivatives within muscle cells, which activate proteins Kinase C-ε and C-θ, ultimately reducing the glucose uptake at any given level of insulin.
Genetics is the highest risk factor.
Perpetual insulin in those who are obese, those receptors become desensitized to the insulin, and become resistant to its effect.

39
Q

What are autosomal dominant diseases

14

A
  1. Achondroplasia,
  2. autosomal dominant polycystic kidney disease,
  3. familial adenomatous polyposis,
  4. familial hypercholesterolemia,
  5. hereditary hemorrhagic telangiectasia,
  6. hereditary spherocytosis,
  7. Huntington disease,
  8. Li-Fraumeni syndrome,
  9. Marfan syndrome,
  10. multiple endocrine neoplasias,
  11. neurofibromatosis type 1 (von Recklinghausen disease),
  12. neurofibromatosis type 2,
  13. tuberous sclerosis,
  14. von Hippel-Lindau disease.
40
Q

Important autosomal recessive diseases

12

A
  1. Albinism,
  2. autosomal recessive polycystic kidney disease (ARPKD),
  3. cystic fibrosis,
  4. glycogen storage diseases, hemochromatosis,
  5. Kartagener syndrome,
  6. mucopolysaccharidoses (except
    Hunter syndrome),
  7. phenylketonuria,
  8. sickle cell anemia,
  9. sphingolipidoses (except Fabry disease),
  10. thalassemias,
  11. Wilson disease.
41
Q

Erythrocyte sedimentation rate

A

The erythrocyte sedimentation rate (ESR or sed rate) is a relatively simple, inexpensive, non-specific test that has been used for many years to help detect inflammation associated with conditions such as infections, cancers, and autoimmune diseases.

The erythrocyte sedimentation rate is the rate at which red blood cells sediment in a period of one hour. It is a common hematology test, and is a non-specific measure of inflammation. Wikipedia

42
Q

Meconium ileus

A

In cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth.

Meconium is the earliest stool of a mammalian infant. Unlike later feces, meconium is composed of materials ingested during the time the infant spends in the uterus: intestinal epithelial cells, lanugo, mucus, amniotic fluid, bile, and water

43
Q

What is normal fetal heart rate

And RR

A
A normal fetal heart rate (FHR) usually ranges from 120 to 160 beats per minute (bpm) in the in utero period. 
The doctor said 200 can still be normal but past that is too fast. 
It is measurable sonographically from around 6 weeks and the normal range varies during gestation, increasing to around 170 bpm at 10 weeks and decreasing from then to around 130 bpm at term.
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Breathing rate (normally 40 to 60 breaths per minute in the newborn period)
44
Q

Neonatal Jaundice

A

At birth, immature UDP-glucuronosyltransferase > unconjugated hyperbilirubinemia > jaundice/
kernicterus (deposition of unconjugated, lipid-soluble bilirubin in the brain, particularly basal
ganglia).
Occurs after first 24 hours of life and usually resolves without treatment in 1–2 weeks.
Treatment: phototherapy (non-UV) isomerizes unconjugated bilirubin to water-soluble form. If left untreated, bilirubin can diffuse into brain, causing toxic encephalopathy (kernicterus)

What is jaundice? (FA)
Abnormal yellowing of the skin and/or sclera due to bilirubin deposition.
Hyperbilirubinemia 2° to increasedproduction or
decreaseddisposition (impaired hepatic uptake, conjugation, excretion).

HOT Liver - common causes of increased levels of bilirubin
Hemolysis
Obstruction 
Tumor 
Liver disease
45
Q

Mycoplasma pneumonia (little boy with pink hair)

A

Classic cause of atypical “walking” pneumonia
(insidious onset, headache, nonproductive
cough, patchy or diffuse interstitial iniltrate). X-ray looks worse than patient.
High titer of cold agglutinins (IgM), which can agglutinate or lyse RBCs. Grown on Eaton agar.
Treatment: macrolides, doxycycline, or
luoroquinolone (penicillin ineffective since Mycoplasma have no cell wall).
No cell wall.

Not seen on Gram stain.
Pleomorphic. Bacterial membrane contains sterols for stability. Mycoplasmal pneumonia is more common in
patients < 30 years old. Frequent outbreaks in military recruits and
prisons. Mycoplasma gets cold without a coat (cell wall).

Sketchy:
Mycoplasma pneumonia - “walking on thin ice”
1. No stain color - Gram indeterminate
2. No walls on the pond for the hockey game - No cell walls, like the pond, so cant appear on gram
stain
3. Net with ringed structures resembling sterols - Cholesterol in the cell membrane, sterols in the
membrane which do not gram stain
4. Referee walking around with no issues - Atypical pneumonia because can’t readily culture a microbe - walking pneumonia. X ray much worse than patients do clinically
5. Patchy collection of clouds in the sky -Patchy infiltrate in the x ray
6. Young players - Young adults, commonly in military recruits. Less than 30 y/o
7. Camouflage goalie <30 – military recruits <30
8. Hockey pucks that are stuck together - IgM molecules that agglutinate red blood cells in cold
temperatures, lysis of RBC’s
9. IgM Snowflakes - IgM
10. Do not EAT ON ice - Grown on eatons agar, “do not eat on ice”
11. Crows - Treatment - Macrolides - Zpack

46
Q

Rh hemolytic disease of newborn

A

IgM does not cross placenta; IgG does cross placenta. Rh⊝ mothers exposed to fetal Rh⊕ blood (often during delivery) may make anti-D IgG. In subsequent pregnancies, anti-D IgG crosses the placenta >hemolytic disease of the newborn
(erythroblastosis fetalis) in the next fetus that is Rh⊕.

Administration of anti-D IgG (RhoGAM)
to Rh⊝ pregnant women during third trimester and early postpartum period prevents maternal anti-D IgG production. Rh⊝ mothers have anti-D IgG only if previously exposed to Rh⊕ blood.

47
Q

ABO hemolytic disease

A

Usually occurs in a type O mother with a type A or B fetus. Can occur in a first pregnancy as maternal anti-A and/or anti-B IgG antibodies may be formed prior to pregnancy. Does not worsen
with future pregnancies. (hemolysis) Presents as mild jaundice in the neonate within 24 hours of birth;
treatment is phototherapy or exchange transfusion.

48
Q

Seizures

A

Characterized by synchronized, high-frequency neuronal firing. Variety of forms.

  1. Partial (focal) seizures
    -Affect single area of the brain. Most commonly originate in medial temporal lobe. Often preceded by seizure aura; can secondarily generalize.
    Types: ƒ Simple partial (consciousness intact)—motor, sensory, autonomic, psychic ƒ
    Complex partial (impaired consciousness)

Generalized seizures Diffuse. Types:
ƒ1. Absence (petit mal)—3 Hz spike-and-wave discharges, no postictal confusion, blank
stare ƒ
2. Myoclonic—quick, repetitive jerk
3. To n i c- c l o n i c (grand mal)—alternating stiffening and movement ƒ
4. To n i c—stiffening ƒ
5. Atonic—“drop” seizures (falls to floor); commonly mistaken for fainting

Epilepsy—a disorder of recurrent seizures (febrile seizures are not epilepsy).

Status epilepticus—continuous (> 5–30 min) or recurring seizures that may result in brain injury. Causes of seizures by age:
ƒChildren—genetic, infection (febrile),
trauma, congenital, metabolic ƒ
Adults—tumor, trauma, stroke, infection ƒ
Elderly—stroke, tumor, trauma, metabolic, infection

49
Q

Levetiracetam (keppra

A

Commonly prescribed anticonvulsant

Use: partial and tonic clonic

Unknown mechanism, may modulate GABA and glutamate relase

Side effects include
-fatigue, drowsiness, headache, neuropsychiatric symptoms (eg personality changes)

50
Q

Dextrocardia vs Situs inversus

A

Situs inversus (also called situs transversus or oppositus) is a congenital condition in which the major visceral organs are reversed or mirrored from their normal positions. The normal arrangement of internal organs is known as situs solitus while situs inversus is generally the mirror image of situs solitus.

You can have isolated dextrocardia not a result of kartegners syndrome and that will be asymptomatic. The child you saw (red hair), had no repositioning of any of the internal organs other than the heart (gas bubble and liver).

51
Q

Peds: asymmetric thigh crease

A

It is a commonly held belief, both amongst health care professionals and the lay public that asymmetrical thigh creases (ATC) in an infant is a sign of developmental dysplasia of the hip (DDH). This study aims to determine whether this finding alone is sufficient to warrant referral to a specialist paediatric orthopaedic surgeon

Its an unreliable clinical sign as 0.5% of such patients going on to require treatme

Thigh folds (seperate from gluteal folds) that are asymmetrical rarely indicate hip dysplasia unless they are associated with uneven gluteal creases. … However this baby’s thigh creases are uneven (note the yellow lines). The left thigh is smooth but the right thigh presents with two creases.

When a baby’s hip dislocation is present for several months, the hips gradually lose range of motion and the leg appears shorter because the hip has migrated upward.

Developmental Dysplasia Of The Hip:

52
Q

Eczema

A

is a group of diseases that results in inflammation of the skin. These diseases are characterized by itchiness, red skin, and a rash.[1] In cases of short duration there may be small blisters while in long-term cases the skin may become thickened.[1] The area of skin involved can vary from small to the entire body.

Dumbed down: Healthy skin helps retain moisture and protects you from bacteria, irritants and allergens. Eczema is related to a gene variation that affects the skin’s ability to provide this protection. This allows your skin to be affected by environmental factors, irritants and allergens.
* Eczema occurs about three times more frequently in individuals with celiac disease and about two times more frequently in relatives of those with celiac disease, potentially indicating a genetic link between the conditions.

In some children, food allergies may play a role in causing eczema.

Risk factors
The primary risk factor for atopic dermatitis is having a personal or family history of eczema, allergies, hay fever or asthma.

1-5 infants have eczema
Aka atopic dermatitis

Complications of dermatitis (eczema) may include:

  • Asthma and hay fever. Eczema sometimes precedes these conditions. More than half of young children with atopic dermatitis develop asthma and hay fever by age 13.
  • Chronic itchy, scaly skin. A skin condition called neurodermatitis (lichen simplex chronicus) starts with a patch of itchy skin. You scratch the area, which makes it even itchier. Eventually, you may scratch simply out of habit. This condition can cause the affected skin to become discolored, thick and leathery.
  • Skin infections. Repeated scratching that breaks the skin can cause open sores and cracks. These increase the risk of infection from bacteria and viruses, including the herpes simplex virus.
  • Irritant hand dermatitis. This especially affects people whose work requires that their hands are often wet and exposed to harsh soaps, detergents and disinfectants.
  • Allergic contact dermatitis. This condition is common in people with atopic dermatitis.
  • Sleep problems. The itch-scratch cycle can cause poor sleep quality.

Treatment of atopic dermatitis is typically with moisturizers and steroid creams.[4] The steroid creams should generally be of mid- to high strength and used for less than two weeks at a time as side effects can occur.[6] Antibiotics may be required if there are signs of skin infection.[2] Contact dermatitis is typically treated by avoiding the allergen or irritant.[7][8] Antihistamines may help with sleep and to decrease nighttime scratching

53
Q

Tinea: peds

corporis, incognito

A

Tinea, or ringworm, is any of a variety of skin mycoses.[1] Tinea is a very common fungal infection of the skin. Tinea is often called “ringworm” because the rash is circular, with a ring-like appearance.

Tinea corporis (also known as “ringworm”,is a superficial fungal infection (dermatophytosis) of the arms and legs, especially on glabrous skin; however, it may occur on any part of the body, it present as annular, marginated plaque with thin scale and clear center. Common organism are Trichophyton mentagrophytes and Micosporum canis. Treatment include : Grisofluvine, itraconazole and clotrimazole cream .

Tinea incognito is a fungal infection (mycosis) of the skin caused by the presence of a topical immunosuppressive agent. The usual agent is a topical corticosteroid (topical steroid). As the skin fungal infection has lost some of the characteristic features due to suppression of inflammation, it may have a poorly defined border, skin atrophy, telangiectasia, and florid growth. Occasionally, secondary infection with bacteria occurs with concurrent pustules and impetigo.[24]

Often the patient and/or their doctor believe they have a dermatitis, hence the use of a topical steroid cream. The steroid cream dampens down inflammation so the condition feels less irritable. But when the cream is stopped for a few days the itch gets worse, so the steroid cream is promptly used again. The more steroid applied, the more extensive the fungal infection becomes and the less recognisable.

Tinea is usually treated with topical antifungals (such as miconazole, ketoconazole, econazole), but if the treatment is unsuccessful, oral antifungal medicines may be considered, including terbinafine and itraconazole. (for example if its tinea capitis and it enters the hair follicle)

Complication: The result is that the original infection slowly extends, the more steroid, the more extensive

54
Q

When can infants get flu vaccine

A

6 months at least,

second a month later

55
Q

Marfan’s diagnosis, treatment

A

If your doctor suspects Marfan syndrome, one of the first tests he or she may recommend is an echocardiogram. This test uses sound waves to capture real-time images of your heart in motion. It checks the condition of your heart valves and the size of your aorta. Other heart-imaging options include computerized tomography (CT) scans and magnetic resonance imaging (MRI).

If you are diagnosed with Marfan syndrome, you’ll need to have regular echocardiograms to monitor the size and condition of your aorta.

Eye tests

Eye exams that may be needed include:

Slit-lamp exam. This test checks for lens dislocation, cataracts or a detached retina. Your eyes will need to be completely dilated with drops for this exam.
Eye pressure test. To check for glaucoma, your eye doctor may measure the pressure inside your eyeball by touching it with a special tool. Numbing eyedrops are usually used before this test.
Genetic testing

If findings from standard exams for Marfan syndrome aren’t clear-cut, genetic testing can be helpful. You may also want to talk to a genetic counselor before starting a family, to see what your chances are of passing on Marfan syndrome to your future children.

Treatment
While there is no cure for Marfan syndrome, treatment focuses on preventing the various complications of the disease. To accomplish this, you’ll need to be checked regularly for signs that the damage caused by the disease is progressing.

In the past, people who had Marfan syndrome rarely lived past 40. With regular monitoring and modern treatment, most people with Marfan syndrome can now expect to live a more normal life span.

Medications

Doctors often prescribe blood pressure lowering drugs to help prevent the aorta from enlarging and to reduce the risk of dissection and rupture. The most commonly used drugs are beta blockers, which cause your heart to beat more slowly and with less force. Losartan (Cozaar), a newer blood pressure medication, also is useful for protecting the aorta.

Therapy

A dislocated lens in your eye can be treated effectively with glasses or contact lenses that refract around or through the lens.

Aortic repair. If your aorta’s diameter enlarges quickly or reaches about 2 inches (5 centimeters), your doctor may recommend an operation to replace a portion of your aorta with a tube made of synthetic material.

This can help prevent a life-threatening rupture. Your aortic valve may need to be replaced as well.
Scoliosis treatment. For some children and adolescents, doctors recommend a custom-made back brace, which is worn nearly continuously until growth is complete. If the curve in your child’s spine is too great, your doctor may suggest surgery to straighten the spine.
Breastbone corrections. Surgical options are available to correct the appearance of a sunken or protruding breastbone. Because these operations are often considered to be for cosmetic purposes, your insurance might not cover the costs.
Eye surgeries. If parts of your retina have torn or come loose from the back of your eye, surgical repair is usually successful. If you have cataracts, your clouded lens can be replaced with an artificial lens

56
Q

why is pulmonary infarct a result of PE is rare?

A

because you are receiving O2 from 1. pulmonary artery, 2. bronchial arteries 3. air

57
Q

What are exam signs of COPD

A
  1. barrel chest
  2. hyper resonance
  3. dull TF
  4. scattered ronchi (low pitched honking sound from mucus)+ wheezing (bronchoconstriction)
  5. very very diminished breath sounds
58
Q

Finger clubbing with pulmonary symptoms?

A

Think malignancy

59
Q

PE with hemoptysis, what is the pathophys?

A
  1. Microclots block a pulmonary/bronchial artery
  2. Infarct*
  3. Hemmorhagic infarct
60
Q

Lipofuscin

A

A yellow-brown “wear and tear” pigment associated with normal aging.

Formed by oxidation and polymerization of autophagocytosed organellar membranes. Autopsy of elderly person will reveal deposits in heart, colon, liver, kidney, eye, and other organs.

61
Q

which conditions are associated with down syndrome (increased risk)

A
  1. Alzheimer disease - amyloid precursor protein is found on chromosome 21
62
Q

which disorders features trinucleotide repeats (important because these can present earlier in subsequent generations)

A
  1. Huntington (AD) - autosomal dominant